This paper summarizes the experience of professor LIU Shangyi in differentiating and treating rectal carcinoma from the perspective of "treating ulcers as tumors". It is believed that the manifestations of rectal cancer， such as anal itching， cauliflower-like or ulcerative tumors， and bloody stools， are similar to external skin itching， skin ulceration， swelling， and skin bleeding. Therefore， the treatment principles of sores and ulcers department can be applied to treat tumors. Following the diagnostic and treatment approach of dermatology regarding the clinical typical symptoms， for anal itching， the main treatment is to dispel wind and remove dampness， clear heat to relieve itching， using "skin medicinals" such as Difuzi （Fructus Kochiae） and Baixianpi （Cortex Dictamni）， as well as wind medicinals such as Shengma （Rhizoma Cimicifugae） and Fangfeng （Radix Saposhnikoviae）. For constipation， the method of clearing heat and resolving toxins， unblocking the bowels and discharging heat can be used， commonly using Baitouweng （Radix Pulsatillae）， Donglingcao （Herba Rabdosiae Rubescentis） and Dahuang （Radix et Rhizoma Rhei）. In terms of mucosal ulcers， it is critical to differentiate between yin and yang； the treatment of yang ulcers should focus on clearing heat and resolving toxins， commonly using modified Xianfang Huoming Beverage （仙方活命饮）； for yin ulcers， emphasis should be placed on removing dampness and resolving phlegm， commonly with modified Yiyi Fuzi Baijiang Powder （薏苡附子败酱散）. For bloody stool， differentiation is made between deficiency and excess， with the use of Diyu （Radix Sanguisorbae） and Huaihua （Flos Sophorae） for excess syndrome to cool and stop blee-ding， and both herbs dry-fried until charred combined with liver-tonifying medicinals for deficiency syndrome

ObjectiveThis study aimed to investigate the action mechanism by which Banxia Xiexintang （BXT） inhibits epithelial-mesenchymal transition （EMT） in chronic atrophic gastritis （CAG） rats by regulating the interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT enhancer binding protein β（C/EBPβ）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas. MethodsA CAG rat model was established by using the combined factor method. After successful modeling， the rats were randomly divided into the model group， low-， medium-， and high-dose groups （0.549， 1.098， 2.196 g·kg^-1， respectively） of BXT， and the positive drug group （vitacoenzyme， 0.3 g·kg^-1）. A normal control group was also set up. After 8 weeks of intervention， the pathological changes of gastric tissue were evaluated. The enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of IL-17， tumor necrosis factor-α （TNF-α）， cyclooxygenase-2 （COX-2）， and C/EBPβ in serum， as well as the contents of EMT markers in gastric mucosal tissue including E-cadherin， N-cadherin， and vimentin. The immunohistochemistry method was employed to determine the localization and protein expression levels of IL-17， p-ERK， and C/EBPβ in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBPβ， ERK， and its phosphorylated form （p）-ERK in gastric mucosa. Real-time polymerase chain reaction （Real-time PCR） was applied to measure the mRNA expression levels of ERK， COX-2， and C/EBPβ in gastric mucosa. ResultsCompared with those in the normal control group， the rats in the model group showed gastric mucosal glandular atrophy and inflammatory cell infiltration. The protein and their related mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly increased （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBPβ in serum were significantly increased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosal tissue were significantly increased， while the content of E-cadherin was significantly decreased （P<0.01）. Compared with the model group， after intervention with different doses of BXT， the pathological damage of the gastric mucosa was improved to varying degrees. The protein and mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly reduced （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBP β in serum were significantly decreased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （P<0.05，P<0.01）. ConclusionBXT can effectively improve the pathological damage of gastric mucosal tissue in CAG rats. Its action mechanism may be related to reducing the levels of IL-17 and TNF-α in serum， regulating the IL-17/ERK/C/EBPβ signaling pathway and inhibiting the EMT process.

Stroke is one of the leading causes of disability and mortality worldwide. Research into its mechanisms and the development of therapeutic strategies heavily rely on animal models that accurately replicate the pathological features of human disease. An ideal animal model for stroke should not only reproduce the neurological deficits and pathological changes observed in clinical patients but also demonstrate good reproducibility and translational value. This review focuses on the preparation and evaluation methods of ischemic stroke animal models. Firstly, it elaborates on the selection criteria, advantages, and disadvantages of experimental animals, including rodents (rats, mice) and non-rodents (non-human primates, miniature pigs, rabbits, zebrafish). Secondly, it provides a detailed overview of the modeling principles, key procedures, and application scopes for ischemic stroke models and hemorrhagic stroke models. Furthermore, the review summarizes advances in the applications of emerging technologies—including gene editing [e.g., clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing], multimodal imaging (e.g., two-photon microscopy, photoacoustic imaging), artificial intelligence, optogenetics, 3D bioprinting, organoid models, and multi-omics–in model optimization, precise assessment, and mechanistic investigation. Finally, based on a systematic analysis of relevant domestic and international literature from 2019 to 2024, this review discusses model selection strategies based on research objectives, a multidimensional evaluation system encompassing behavioral, imaging, and molecular pathological assessments, and envisions future directions involving technological integration to achieve model precision and individualization. This article aims to provide a comprehensive methodological reference to help researchers select appropriate animal models of stroke according to specific scientific questions.

This paper explores the immune-inflammatory regulatory mechanism of colorectal cancer cachexia and corresponding traditional Chinese medicine （TCM） intervention strategies based on the TCM theory of reinforcing healthy qi and dispelling pathogenen. It is proposed that depletion of healthy qi is the root cause of colorectal cancer cachexia， while cancer toxins exuberance is the symptomatic manifestation of the disease， and failure of the spleen and stomach is the core pathogenesis. In terms of treatment， a TCM treatment system is constructed based on the principles of reinforcing healthy qi to consolidate the foundation and regulate immunity， and dispelling pathogen to remove toxins and alleviate inflammation. The system clarifies the healty qi-reinforcing method as fortifying spleen and boosting qi to enhance immune function， and nourishing blood and enriching yin to consolidate yin essence and healthy qi. It also emphasizes the pathogen-dispelling method as clearing heat and removing toxins to regulate the secretion of inflammatory cytokines， and promoting blood circulation and resolving stasis to improve the immune microenvironment and microcirculation. This therapeutic approach may provide valuable insights for TCM interventions in colo-rectal cancer cachexia.

Lipid turbidity disease is a metabolic disease featuring lipid metabolism disorders caused by many factors such as social environment， diet， and lifestyle， which is closely related to many diseases in modern medicine， such as hyperlipidemia， obesity， fatty liver， atherosclerosis， metabolic syndrome， and cardiovascular and cerebrovascular diseases， with a wide range of influence and far-reaching harm. According to the Huangdi Neijing， lipid turbidity disease reflects the pathological change of the body's physiologic grease. Grease is the thick part of body fluids， which has the function of nourishing， and it is the initial state and source of important substances in the human body such as brain， marrow， essence， and blood. Once the grease of the human body is abnormal， it can lead to lipid turbidity disease. The Huangdi Neijing also points out the physiological relationship between the transportation and transformation of body fluids and the rise and fall of the spleen and stomach， which can deduce the pathological relationship between the occurrence of lipid turbidity disease and the abnormal rise and fall of the spleen and stomach functions. Lipid turbidity disease is caused by overconsumption of fatty and sweet foods or insufficient spleen and stomach endowments， leading to disorders of the function of promoting clear and reducing turbidity in the spleen and stomach. This leads to the transformation of thick grease in body fluids into lipid turbidity， which accumulates in the body's meridians， blood vessels， skin pores， and organs， forming various forms of metabolic diseases. The research team believed that the pathological basis of lipid turbidity disease was the abnormal rise and fall of the spleen and stomach and the obstruction of the transfer of grease. According to the different locations where lipid turbidity stays， it was divided into four common pathogenesis types： ''inability to distinguish between the clear and turbid， turbid stagnation in the Ying blood''， ''spleen not rising clear， turbid accumulation in the vessels''， ''spleen dysfunction， lipid retention in the pores''， ''spleen failure to transportation and transformation， and grease accumulation in the liver''. According to the pathogenesis， it could be divided into four common syndromes， namely， turbid stagnation in the Ying blood， turbid accumulation in the vessels， lipid retention in the pores， and grease accumulation in the liver， and the corresponding prescriptions were given for syndrome differentiation and treatment， so as to guide clinical differentiation and treatment of the lipid turbidity disease.

Artificial intelligence (AI) technologies are being widely applied in radiotherapy. However, the integration of AI into clinical workflows of radiotherapy faces a series of challenges, such as poor model interpretability, domain shifts between clinical application and training data, and the inherent model uncertainties. Therefore, case-specific quality assurance (QA) is essential before deploying AI models in clinical practice. This paper reviews and summarizes QA methodologies for the application of AI models in radiotherapy across four key areas: image registration, image generation, region of interest segmentation, and treatment planning.

Objective:To compare the efficacy and safety of a domestic hair follicle extraction system versus traditional follicular unit excision (FUE) in extracting hair follicles for the treatment of androgenetic alopecia (AGA) .Methods:A multicenter, randomized, self-controlled clinical trial was conducted on AGA patients aged 18 - 59 years who were recruited from the Huashan Hospital, Fudan University, the Affiliated Hangzhou First People's Hospital, and the China-Japan Friendship Hospital between June 2023 and September 2024. Each patient's scalp was randomly divided into two sides (experimental side vs. control side) using an envelope method. The experimental side underwent robotic hair transplantation with a domestic hair follicle extraction system, and the control side underwent traditional FUE. Hair follicles were extracted from the safe donor area in the occipital region, and implanted into the ipsilateral hair loss area. The primary outcome was the hair transection rate which was calculated immediately after follicular extraction. The secondary outcomes included the hair follicle unit loss rate and the change in hair density at the recipient site on postoperative day 14. Safety was evaluated by assessing the incidence of folliculitis at the donor site on postoperative day 14 and the overall incidence of adverse events. Surgical outcomes were evaluated at 9 months after surgery. Comparisons of evaluation indicators among groups were performed by using a paired t test or Wilcoxon signed-rank test. Results:A total of 55 patients with AGA (51 males and 4 females, aged 32.71 ± 5.75 years) completed the hair follicle transplantation and postoperative follow-up. The hair transection rate ( M[ Q1, Q3]) was 6.65% (4.56%, 10.16%) in the experimental group and 5.28% (3.04%, 8.89%) in the control group (difference = 1.24%, 95% CI: -0.24%, 2.65%) . The hair follicle unit loss rate was 2.00% (1.00%, 3.50%) in the experimental group and 0.50% (0, 2.00%) in the control group, with a significant difference between the two groups ( P = 0.008) . On postoperative day 14, there was no significant difference in the hair density between the experimental group and control group (72.20 ± 25.95 per cm 2vs. 76.49 ± 30.84 per cm 2, P = 0.173) . At 9-month follow-up, both groups showed improvement in the investigator's overall score in the recipient areas. Seven adverse events occurred in 7 subjects (12.72%) in each group, and all were mild folliculitis. Conclusion:The domestic hair follicle extraction system demonstrated comparable efficacy and safety to the traditional FUE in hair transplantation.

Changes in hair follicle stem cells (HFSCs) can affect scalp aging and hair growth. With increasing age, HFSCs exhibit a decrease in quiescence maintenance and self-renewal capacity, as well as differentiation potential, leading to shortened hair growth cycles and even hair loss. This review summarizes recent research advances in the multifactorial interactions underlying hair loss, including the regulatory mechanisms of HFSC quiescence, the impact of aging on HFSC function, and aging of the stem cell microenvironment. Additionally, this review discusses the relationship between stem cells and hair shafts, and the mechanisms of action of stem cells in scalp aging, including alterations in signaling pathways, chromatin remodeling, and epigenetic regulation, etc. Furthermore, stem cell-based therapeutic strategies are summarized, such as the use of stem cells or their secreting exosomes, modulation of the stem cell microenvironment, and pharmacological interventions.

Topical minoxidil has been applied to the treatment of androgenetic alopecia (AGA) in clinical practice for a long time, but some problems still exist, such as unsatisfactory efficacy or poor tolerance. Currently, oral minoxidil is only indicated as second- or third-line therapy for hypertension, but growing evidence has supported the off-label use of low-dose oral minoxidil for the treatment of AGA. This review summarizes possible mechanisms and clinical application of low-dose oral minoxidil in the treatment of AGA.

OBJECTIVES: The integrated endoplasmic reticulum stress inhibitor (ISRIB) is a selective inhibitor of the protein kinase R-like endoplasmic reticulum kinase (PERK) signaling pathway within endoplasmic reticulum stress (ERS) and can improve spatial and working memory in aged mice. Although ERS and oxidative stress are tightly interconnected, it remains unclear whether ISRIB alleviates cognitive impairment by restoring the balance between ERS and oxidative stress. This study aims to investigate the effects and mechanisms of ISRIB on lipopolysaccharide (LPS)-induced cognitive impairment in mice. METHODS: Eight-week-old male ICR mice were randomly divided into 3 groups: Normal saline (NS) group, LPS group, and ISRIB+LPS group. NS and LPS groups received daily intraperitoneal injections of normal saline for 7 days; on day 7, LPS group mice received intraperitoneal LPS (0.83 mg/kg) to establish a cognitive impairment model. ISRIB+LPS group received ISRIB (0.25 mg/kg) intraperitoneally for 7 days, with LPS injected 30 minutes after ISRIB on day 7. Cognitive ability was evaluated by the novel place recognition test (NPRT). Real-time fluorogenic quantitative PCR (RT-qPCR) was used to detect changes in nitric oxide synthase (NOS), superoxide dismutase-1 (SOD-1), and catalase (CAT) gene expression in the hippocampus and prefrontal cortex. Oxidative stress markers malondialdehyde (MDA), glutathione (GSH), and oxidized glutathione (GSSG), were measured in hippocampal and prefrontal cortex tissues. RESULTS: Compared with the NS group, mice in LPS group showed a significant reduction in novel place recognition ratio, upregulation of hippocampal NOS-1 and NOS-2 mRNA, downregulation of SOD-1 and CAT mRNA, increased MDA and GSSG, decreased GSH, and reduced GSH/GSSG ratio (all P<0.05). Compared with the LPS group, mice in ISRIB+LPS group exhibited significantly improved novel place recognition, downregulated NOS-1 and NOS-2 mRNA, upregulated SOD-1 and CAT mRNA, decreased MDA and GSSG, increased GSH, and an elevated GSH/GSSG ratio in the hippocampus (all P<0.05). No significant changes were observed in the prefrontal cortex. CONCLUSIONS ISRIB improves LPS-induced cognitive impairment in mice by restoring the oxidative/antioxidant balance in the hippocampus.
Animals ; Lipopolysaccharides ; Male ; Mice, Inbred ICR ; Cognitive Dysfunction/drug therapy* ; Mice ; Oxidative Stress/drug effects* ; Endoplasmic Reticulum Stress/drug effects* ; Hippocampus/drug effects* ; Nitric Oxide Synthase Type II/genetics* ; Guanidines/pharmacology* ; eIF-2 Kinase/antagonists & inhibitors* ; Signal Transduction/drug effects* ; Superoxide Dismutase/metabolism*