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.

This article adopts Professor CHEN Chaozu′s " sanjiao composed by membrane-striae" theory as its foundation to explore the relationship between irritable bowel syndrome and functional/structural abnormalities of the membrane-striae. Sanjiao encompasses both the tangible membrane and the intangible striae. These striae permeate the entire body，and their pathological changes comprehensively reflect qi，body fluids，and fasciae. Based on the physiological function of the membrane-striae in regulating qi and fluids，the pathogenesis of irritable bowel syndrome is characterized by a disharmony of membrane-striae and an imbalance of the qi-fluid interactions. In the early stage，external pathogens，emotional factors，or dietary stimuli often cause membrane-striae constriction and disordered qi-fluid circulation. In the middle stage，stagnant fluids gradually transform into phlegm retention，leading to membrane-striae obstruction. In the late stage，deficiency of vital qi becomes predominant，manifesting as laxity of membrane-striae with impaired control or weakened conduction. The treatment of irritable bowel syndrome should adopt " unblocking" as the guiding principle. In the early stage，therapy should focus on eliminating pathogenic factors and soothing membrane-striae to promptly restore qi-fluid circulation，thereby attaining unblocking through spasm relief. In the middle stage，treatment should focus on resolving tangible obstructions in membrane-striae，achieving unblocking via dredging. In the late stage，the emphasis should shift to reinforcing healthy qi，particularly by strengthening spleen-kidney yang qi，and achieving unblocking through supplementation. Concurrently，throughout the entire treatment process，the regulation of mental state and easing of emotional tension should be integrated to alleviate patient′s anxiety，achieving the goal of holistic treatment of both body and mind.

Lung cancer remains one of the leading causes of cancer-related morbidity and mortality worldwide, and its treatment continues to face major challenges such as therapeutic resistance and tumor recurrence. Pyroptosis, a newly characterized form of programmed cell death, induces tumor cell death through gasdermin-mediated membrane pore formation and is accompanied by the release of inflammatory mediators, thereby playing complex roles in lung cancer initiation, progression, and modulation of the tumor microenvironment. Active components and herbal formulas derived from traditional Chinese medicine can modulate pyroptosis-related signaling pathways through multi-target mechanisms, showing potential advantages in inducing lung cancer cell death, inhibiting proliferation and migration, and reversing chemoresistance. This review systematically summarizes relevant studies from domestic and international sources, focusing on the molecular mechanisms of pyroptosis, its roles in lung cancer development and tumor microenvironment remodeling, and the current research progress on traditional Chinese medicine-based interventions targeting pyroptosis, with the aim of providing references for the prevention and treatment of lung cancer using traditional Chinese medicine.

ObjectiveTo compare female C57BL/6J and BALB/c mice models of ulcerative colitis (UC) induced by dextran sulfate sodium salt (DSS), providing a reference for selecting female animal models in studies of innovative drugs for UC treatment. MethodsA total of 48 female mice aged 6–8 weeks, including 24 C57BL/6J and 24 BALB/c mice, were divided into four groups: control group, UC-3d group (2.5% DSS drinking for 3 days), UC-7d group (2.5% DSS drinking for 7 days), and UC-withdrawal group (2.5% DSS drinking for 7 days followed by 3 days of pure water replacement), with 6 mice in each group. Body weight, fecal occult blood, and stool characteristics were recorded daily, and disease activity index (DAI) scores were calculated. At the end of DSS induction, mice were gavaged with fluorescein isothiocyanate (FITC)-labeled dextran solution before tissue collection. Four hours later, under deep anesthesia induced by inhalation of 4% isoflurane, blood samples were collected from the retro-orbital venous plexus, and euthanasia was performed by cervical dislocation. The colon was then separated immediately, and its length from the anus to the ileocecal junction was measured. Colon tissues were fixed, embedded, and sectioned, and they were evaluated using hematoxylin-eosin (HE) staining and alcian blue-periodic acid-Schiff (AB-PAS) staining to comprehensively assess the degree of colonic inflammation. The spleen was also collected and weighed, and the spleen coefficient was calculated. Serum FITC fluorescence intensity and D-lactic acid concentration were measured to evaluate intestinal permeability and barrier injury. The grooming duration, the number of buried marbles, the time spent in the center of the open field, and the total distance traveled were measured to evaluate anxiety/depression-like behaviors in mice. ResultsFecal occult blood appeared in both C57BL/6J and BALB/c mice after 3 days of ad libitum access to DSS. Compared with the control group, there was no significant change in the weight loss rate of female BALB/c mice in the UC-7d and UC-withdrawal groups (P > 0.05), but the DAI score increased (P < 0.01). Conversely, both the weight loss rate and DAI score increased for female C57BL/6J mice in the UC-7d and UC-withdrawal groups (P < 0.01). In female C57BL/6J mice, both the UC-7d and UC-withdrawal groups had higher spleen coefficients than the control group (P < 0.05). Additionally, in these groups, colon length was significantly reduced (P < 0.01), FITC fluorescence intensity in serum was markedly increased (P < 0.01), obvious inflammatory reaction areas appeared in the colon, and the goblet cells and acidic mucus layer were damaged. In contrast, in female BALB/c mice, no significant differences were observed in colon length, serum FITC fluorescence intensity, or D-lactic acid concentration between the UC-7d and UC-withdrawal groups compared with the control group (P > 0.05). Only a few inflammatory cells and damaged goblet cells were observed in the colonic mucosal layer, and no other obvious pathological changes were detected. In addition, female C57BL/6J mice in the UC-7d group showed a significantly reduced total distance in the open field and fewer buried marbles (P < 0.05), indicating depression-like behavior, as well as prolonged grooming duration (P < 0.05), indicating anxiety-like behavior. ConclusionFemale BALB/c mice are not sensitive to 2.5% DSS and do not show typical colonic pathological changes of UC. In contrast, ad libitum access to 2.5% DSS for 7 days successfully induces typical UC pathological symptoms and colonic pathological changes in female C57BL/6J mice. These changes persist for 3 days after DSS withdrawal, and the mice also exhibit symptoms of anxiety/depression. The results suggest that this model can be used for research on the pathogenesis and therapeutic drugs of UC.

ObjectiveThe present study aimed to investigate alterations in white matter microstructure and spontaneous neural activity in male college smokers, and to further explore their associations with nicotine dependence. Given that adolescence and early adulthood represent critical periods for brain maturation, particularly for white matter development, understanding the neural correlates of smoking behavior during this stage is of substantial importance for both neuroscience and public health. MethodsA total of 115 male undergraduate students were initially recruited for this study. After quality control and exclusion procedures, 52 male college smokers and 42 demographically matched healthy non-smokers were included in the final analysis. All participants underwent multimodal magnetic resonance imaging (MRI), including diffusion tensor imaging (DTI) and resting-state functional MRI (rs-fMRI). White matter fiber tracts were reconstructed using the automated fiber quantification (AFQ) method, which enables precise identification and quantification of major fiber bundles. Eighteen major white matter tracts were segmented for each participant. Along the core trajectory of each tract, 100 equidistant nodes were sampled. Fractional anisotropy (FA) was calculated at each node to assess white matter microstructural integrity, while amplitude of low-frequency fluctuation (ALFF) was computed to evaluate spontaneous neural activity within white matter tracts. Between-group differences in FA and ALFF were assessed using two-sample t-tests, with appropriate corrections applied for multiple comparisons. Furthermore, Pearson correlation analyses were conducted to examine the relationships between imaging-derived metrics (FA and ALFF values in regions showing significant group differences) and nicotine dependence severity, as measured by the Fagerström test for nicotine dependence (FTND). ResultsCompared with healthy non-smokers, male college smokers exhibited significantly increased FA values in several white matter tracts, including the left thalamic radiation, right corticospinal tract, forceps major of the corpus callosum, left uncinate fasciculus, and right arcuate fasciculus. These findings suggest altered microstructural organization or increased directional coherence within these pathways. In addition, smokers demonstrated significantly elevated ALFF values in the forceps major, right uncinate fasciculus, and left arcuate fasciculus, indicating enhanced spontaneous neural activity in these white matter regions. Correlation analyses revealed that FA values in the left thalamic radiation and right corticospinal tract were negatively correlated with FTND scores, suggesting that higher levels of nicotine dependence were associated with reduced microstructural integrity or altered fiber organization in these regions. In contrast, ALFF values in the forceps major and right uncinate fasciculus were positively correlated with FTND scores, indicating that greater nicotine dependence was associated with increased spontaneous neural activity in specific white matter pathways. ConclusionThe present study provides evidence that male college smokers exhibit distinct alterations in both white matter microstructure and functional activity. These abnormalities are not uniformly distributed but rather localized to specific fiber tracts implicated in sensorimotor processing, interhemispheric communication, and higher-order cognitive and emotional regulation. Importantly, the observed associations between imaging metrics and nicotine dependence severity suggest that these structural and functional alterations may reflect neurobiological mechanisms underlying addiction. The combination of AFQ-based tract profiling and multimodal MRI offers a sensitive approach for detecting subtle changes along white matter pathways, highlighting its potential utility in identifying neuroimaging biomarkers of nicotine dependence. Overall, these findings indicate that smoking during early adulthood may disrupt ongoing white matter maturation, potentially leading to long-term consequences for brain function. This study provides novel insights into the neural basis of nicotine dependence and underscores the importance of early intervention and prevention strategies targeting young smokers.

Objective To compare the dosimetric differences, plan complexity, verification pass rate, and execution efficiency of volumetric modulated arc therapy (VMAT) plans designed for post-mastectomy radiotherapy of breast cancer using Halcyon 2.0 and VitalBeam accelerators in flattening filter-free mode. Methods A retrospective analysis was conducted on imaging data from 87 female breast cancer patients aged 29 to 75 (49.9 ± 9.9) years who underwent modified radical mastectomy followed by radiotherapy. VMAT plans were designed using both VitalBeam and Halcyon accelerators in flattening filter-free mode. The dosimetric parameters, plan complexity, verification pass rate, and execution efficiency were compared between the plans designed for both accelerators, with a significance level of P<0.05. Results In terms of target volume parameters, Halcyon 2.0 plans demonstrated superior homogeneity index and conformity index. For organs at risk, the Halcyon 2.0 plans showed lower doses for the lungs (D_20% and D_mean) and heart (D_mean) compared to the VitalBeam plans (all P<0.05). Regarding plan complexity, Halcyon 2.0 plans exhibited better median average aperture area variation (0.35 ± 0.02), smaller aperture score, and larger median plan aperture area than VitalBeam plans (all P<0.05). However, VitalBeam plans had a superior median modulation complexity score (0.28 ± 0.01) compared to Halcyon 2.0 plans (P<0.05). Patient plans were assessed using the ArcCHECK phantom, revealing higher pass rates and significantly shorter execution time for Halcyon plans compared to VitalBeam plans (P<0.05). Conclusion Both Halcyon 2.0 and VitalBeam accelerators can provide high-quality VMAT plans for postoperative radiotherapy of breast cancer, with excellent verification pass rates ensuring treatment accuracy and efficacy. However, Halcyon 2.0 offers lower plan complexity, simplifies the treatment planning process, and reduces execution time, thereby achieving higher treatment efficiency and demonstrating greater advantages in clinical applications.

ObjectiveTo investigate the therapeutic effect and mechanism of modified Chunzetang on bladder fibrosis and detrusor function in rats with neurogenic bladder urinary retention induced by spinal cord injury. MethodsIn this study， an improved Hassan Shaker spinal cord transection method was used to establish a model of neurogenic bladder urinary retention induced by spinal cord injury， and rats with a spinal cord injury behavior score of 0 were selected for follow-up experiments. The selected rats were randomly divided into a model group （normal saline gavage）， low-dose traditional Chinese medicine （TCM） group （gavage of 14.4 g·kg^-1 modified Chunzetang）， high-dose TCM group （gavage of 28.8 g·kg^-1 modified Chunzetang）， positive drug group ［intraperitoneal injection of 0.05 g·kg^-1 nuclear transcription factor-κB （NF-κB） inhibitor pyrrolidine dithiocarbamate （PDTC）］， and combination group （intraperitoneal injection of 0.05 g·kg^-1 PDTC + gavage of 28.8 g·kg^-1 modified Chunzetang）. The rats in these groups were administrated with corresponding drugs once a day for four weeks. The BL-420s biofunction acquisition system was used in the experiment to calculate the urodynamic indexes， and the isolated bladder was quickly weighed. The detrusor traction experiment was used to record the minimum bladder contraction tension and frequency in each group. The pathological morphology and tissue fibrosis of detrusor in each group observed by Hematoxycin-eosin （HE） staining and Masson staining were compared. The expression level of α-smooth muscle actin （α-SMA） was detected by immunohistochemistry. Western blot was used to detect the protein expression of NF-κB p65， nuclear transcription factor-κB suppressor protein α （IκBα）， transforming growth factor-β₁ （TGF-β₁）， type Ⅰ collagen （ColⅠ）， and type Ⅲ collagen （ColⅢ） in bladder tissue of rats in each group. Enzyme-linked immunosorbent assay （ELISA） was used to detect the changes in serum levels of IL-6， IL-1β， and TNF-α. ResultsCompared with that in the sham operation group， the pressure at the urinary leakage point in the model group decreased （P<0.01）， and the bladder mass， bladder contractile tension， maximum bladder capacity， and bladder compliance increased （P<0.05，P<0.01）. HE staining showed that the arrangement of bladder epithelial cells was disordered， and the pathological manifestations such as mucosa and myometria neutrophil infiltration were obvious. The lamina propria structure was destroyed， and the muscle fiber arrangement was disordered. The interstitial widening and tissue edema were obvious. Masson staining showed that the bladder wall of the model group had more collagen fiber deposition， and the degree of detrusor fibrosis was more severe. The content of detrusor in the visual field was reduced. At the same time， the protein expressions of NF-κB p65， TGF-β₁， IκBα， ColⅠ， and ColⅢ in bladder tissue of rats in the model group were significantly increased （P<0.01）， and the serum levels of IL-6， IL-1β， and TNF-α were significantly increased （P<0.05）. Compared with that in the model group， the pressure at the urinary leakage point in the modified Chunzetang and positive drug groups was increased （P<0.05）， and the wet bladder weight， minimum bladder contractile tension， maximum bladder capacity， and bladder compliance were restored （P<0.05， P<0.01）. HE and Masson showed that the bladder epithelial cells were relatively neatly arranged， and the structure of the bladder lamina propria was relatively stable. The detrusor bundles were arranged in an orderly manner， and the interstitium was narrow. The degree of tissue edema was relatively low， and the degree of bladder detrusor fibrosis in the modified Chunzetang and positive drug groups was reduced， while the degree of bladder detrusor fibrosis in the positive drug group and combination groups was not obvious. The results of Western blot showed that the expression of NF-κB p65， IκBα， TGF-β₁， ColⅠ， and ColⅢ in bladder tissue， as well as the serum levels of IL-6， IL-1β， and TNF-α in modified Chunzetang and positive drug groups were significantly lower， and the expression of bladder tissue-related proteins and the serum levels of IL-6， IL-1β， and TNF-α in the TCM groups decreased significantly with the increase in dose （P<0.05）. The results of immunohistochemistry suggested that modified Chunzetang could fully affect the expression of α-SMA in bladder tissue. ConclusionModified Chunzetang can inhibit collagen deposition in bladder tissue of rats with urinary retention induced by spinal cord injury， delay the occurrence and development of bladder fibrosis， and protect the normal contractile function of bladder detrusor， and its mechanism may be related to inhibiting the NF-κB/TGF-β₁ signaling pathway， reducing the production of NF-κB p65， IκBα， TGF-β₁， ColⅠ， ColⅢ， and other related proteins， and protecting the muscle strength of detrusor.

Objective To analyze the proportion and clinicopathological characteristics of HER2-positive breast cancer patients with BRCA1/2 pathogenic variants, and their response to neoadjuvant anti-HER2 targeted therapy. Methods The clinicopathological data of 531 breast cancer patients with germline BRCA1/2 pathogenic variants (201 with BRCA1 variants and 330 with BRCA2 variants) were analyzed. Results Among the 201 BRCA1 and 330 BRCA2 variants, 17 (8.5%) and 42 (12.7%) HER2-positive breast cancer cases were identified, respectively, accounting for 11.1% of all BRCA1/2-mutated breast cancers. Compared with BRCA1/2-mutated HR-positive/HER2-negative patients, HER2-positive patients did not present any significant differences in clinicopathological features; however, compared with triple-negative breast cancer patients, HER2-positive patients had a later onset age and lower tumor grade. Among the 17 patients who received neoadjuvant anti-HER2 targeted therapy, 10 cases achieved pCR (58.8%), whereas 7 cases did not (41.2%). Conclusion HER2-positive breast cancer accounts for more than 10% of BRCA1/2-mutated patients. Approximately 40% of these patients fail to achieve pCR after neoadjuvant targeted therapy. This phenomenon highlights the possibility of combining anti-HER2 targeted agents with poly (adenosine diphosphate-ribose) polymerase inhibitors.

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

Metabolic-associated fatty liver disease (MAFLD) and osteoporosis (OP) are two very common metabolic diseases. A growing body of experimental evidence supports a pathophysiological link between MAFLD and OP. MAFLD is often associated with the development of OP. Rutaecarpine (RUT) is one of the main active components of Chinese medicine Euodiae Fructus. Our previous studies have demonstrated that RUT has lipid-lowering, anti-inflammatory and anti-atherosclerotic effects, and can improve the OP of rats. However, whether RUT can improve both fatty liver and OP symptoms of MAFLD mice at the same time remains to be investigated. In this study, we used C57BL/6 mice fed a high-fat diet (HFD) for 4 months to construct a MAFLD model, and gave the mice a low dose (5 mg·kg^-1) and a high dose (15 mg·kg^-1) of RUT by gavage for 4 weeks. The effects of RUT on liver steatosis and bone metabolism were then evaluated at the end of the experiment [this experiment was approved by the Experimental Animal Ethics Committee of Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences (approval number: IMB-20190124D₃03)]. The results showed that RUT treatment significantly reduced hepatic steatosis and lipid accumulation, and significantly reduced bone loss and promoted bone formation. In summary, this study shows that RUT has an effect of improving fatty liver and OP in MAFLD mice.