This paper explores the differentiation and treatment strategies for pediatric IgA vasculitis based on the correlation between blood trubidity theory and oxidative stress. It is proposed that pediatric IgA vasculitis follows an evolution of pathogenesis characterized by "deficiency of healthy qi leading to turbidity generation， accumulation of turbid toxin， and toxin damage to the collateral vessels"， which corresponds to the pathological process of oxidative stress， namely decreased antioxidant capacity with accumulation of reactive oxygen species， metabolite deposition， and endothelial cell injury. A staged treatment strategy is proposed. In the acute stage， wind-toxin invading the colla-terals and reckless movement of heat in the blood are the main manifestations， for which the treatment should focus on dispelling wind and venting pathogens， resolving toxins and unblocking the collaterals， with a modified Yinqiao Powder （银翘散） and Xijiao Dihuang Decoction （犀角地黄汤） to regulate oxidative stress burst. In the prolonged stage， intermingling of turbidity and stasis with collateral obstruction is emphasized； treatment should focus on resolving turbidity and dispelling stasis， harmonizing the blood and stabilizing the collaterals， and a modified Simiao Powder （四妙散） and Taohong Siwu Decoction （桃红四物汤） can be used to improve microcirculatory dysfunction. In the remission stage， when healthy qi remains insufficient and residual pathogens persist， treatment should focus on strengthening the root and clearing the source， reinforcing healthy qi and nourishing the collaterals， for which modified Zhibai Dihuang Pill （知柏地黄丸） and Yupingfeng Powder （玉屏风散） is suggested to rebuild the antioxidant defense system.

As one of the common systemic vasculitides in children， IgA vasculitis is closely associated with the interaction of "Wind pathogen" and "turbid stasis" in its pathogenesis. Based on the blood turbidity theory， this paper proposes "wind agitating blood turbidity and collateral damage" as the core pathogenesis. Regarding treatment， the sequential therapeutic principle of "stanch bleeding， activating blood circulation， and nourishing blood" is adopted， and combined with the dynamic application of wind-dispelling medicinals to "expel， search， and guard against wind"， turbidity-removing method is applied throughout all stages. In the acute stage，it is recommended to clear heat and purify turbidity， stanch bleeding and secure the collaterals. In the prolonged stage， the method of dissipating stasis and clearing up turbidity should be used， as well as activating blood circulation and unblocking the collaterals. In the recovery stage， it is advised to nourish blood to flourish the collaterals， reinforce healthy qi and resolve turbidity. This therapeutic system integrates the elimination of pathogens and the reinforcement of healthy qi to clear and resolve blood turbidity， ultimately achieving holistic collateral repair through securing， unblocking， and nourishing the collaterals， which provides new insights into the treatment of this disease in traditional Chinese medicine.

ObjectiveTo systematically investigate the medication rules of chicken-derived medicinals for treating children enuresis in ancient Chinese medical classicals. MethodsThe China Medical Classics V5.0 database was searched to identify formulas and passages containing chicken-derived medicinals for pediatric enuresis. A database was established using Microsoft Excel 2021 to extract information including formulas， therapeutic categories， natures， flavors， channel entry， processing methods， dosage forms， and administration methods. Frequency analysis was performed， while association rule analysis and cluster analysis were conducted using R software. Gephi 0.10.1 software was used for complex network analysis. ResultsA total of 171 records were included， comprising 36 single-herb formulas and 135 compound formulas， sourced from 64 classical medical monographs. The identified chicken-derived medicinals included jichang （Intestinum Galli）， jineijin （Endothelium Corneum Gigeriae Galli）， jigan （Gallina Hepar）， jishibai （Faeces Galli Albi）， jisu （Ingluvies Galli）， jiheling （Pluma Alae Galli）， and jiweimao （Chicken tail feathers）. The top three frequently used single herbs were jichang （17 times）， jineijin （8 times）， and jiheling （5 times）. Among compound prescriptions， the three most frequently recorded formulas were Jineijin Powder （鸡内金散， 43 times）， Jichang Powder （鸡肠散， 25 times）， and Guigan Pills （桂肝丸， 24 times）， with jineijin， jichang， and jigan being the predominant chicken-derived medicinals. When converting the daily dosage of chicken-derived medicines into modern dosage units， the dose ranged from 0.53 g to 33.57 g for jineijin， with 4.48 g being the most frequently used dose， and from 0.25 g to 30.00 g for jichang， with 17.90 g being the most frequently used dose. Chicken-derived medicinals were mostly used after processing， commonly employing burning （68 times）， roasting/ stir-baking （37 times）， and calcining （24 times） to preserve properties. Powders （117 times）， pills （45 times）， and decoctions （9 times） were the principal dosage forms， and administration with wine （70 times） was the most common method. The most frequently used herbal pair was jineijin and roucongrong （Herba Cistanches）， while the core prescription combinations were Tusizi Powder （菟丝子散）， Yangshi Jichang Powder （杨氏鸡肠散）， and Rongxiang Pill （茸香丸）. ConclusionChicken-derived medicinals ， such as jichang and jineijin， are commonly processed by burning or roasting before use in the treatment of enuresis. They are often combined with longgu （Fossilia Ossis Mastodi）， muli （Concha Ostreae）， sangpiaoxiao （Oötheca Mantidis）， roucongrong and rougui （Cortex Cinnamomi） to warm and tonify the kidney qi， arrest enuresis and emission with astringents. Pills and powders are the predominant dosage forms and are commonly administered before meals with wine or salted water.

Based on the view that wind pathogen runs through the entire course of the occurrence and development of nephrotic syndrome， it is proposed that the core pathogenesis of refractory nephrotic syndrome （RNS） in children involves imbalance of the lung， spleen， and kidney， invasion of wind pathogen， and stagnation of turbidity and stasis， and that directing the turbid downward with wind medicinals is the key therapeutic strategy. In clinical practice， according to the distinct pathogenic characteristics of three patterns， including defensive qi insecurity of the lung， yang deficiency with loss of regulation， and binding of turbidity and stasis， three corresponding methods are applied， which are diffusing the lung to consolidate defensive qi， elevating yang to supplement the spleen and kidney， and activating blood to unblock turbidity and stasis. For the pattern of defensive qi insecurity of the lung， wind medicinals are used to penetrate and disperse external pathogens， such as fangfeng （Radix Saposhnikoviae） and mahuang （Herba Ephedrae） for diffusing the lung， dispersing wind， and consolidating defensive qi. For yang deficiency with loss of regulation pattern， wind medicinals are employed to elevate yang and assist transformation， such as shengma （Rhizoma Cimicifugae） and gegen （Radix Puerariae Lobatae） for raising clear yang， warming and activating the spleen and kidney. For binding of turbidity and stasis pattern， wind medicinals with scurrying and collateral‑unblocking properties are used， such as jixueteng （Caulis Spatholobi）， luoshiteng （Caulis Trachelospermi）， and chuanshanlong （Rhizoma Dioscoreae Nipponicae） for dispelling wind， activating blood， resolving stasis， and directing turbidity downward. In all these methods， the core principle is to use wind medicinals to regulate qi movement， open and unblock the sweat pores， and separately eliminate turbid pathogens， thereby providing a theoretical and practical basis for the traditional Chinese medicine diagnosis and treatment of RNS in children.

Based on the view that wind pathogen runs through the entire course of the occurrence and development of nephrotic syndrome， it is proposed that the core pathogenesis of refractory nephrotic syndrome （RNS） in children involves imbalance of the lung， spleen， and kidney， invasion of wind pathogen， and stagnation of turbidity and stasis， and that directing the turbid downward with wind medicinals is the key therapeutic strategy. In clinical practice， according to the distinct pathogenic characteristics of three patterns， including defensive qi insecurity of the lung， yang deficiency with loss of regulation， and binding of turbidity and stasis， three corresponding methods are applied， which are diffusing the lung to consolidate defensive qi， elevating yang to supplement the spleen and kidney， and activating blood to unblock turbidity and stasis. For the pattern of defensive qi insecurity of the lung， wind medicinals are used to penetrate and disperse external pathogens， such as fangfeng （Radix Saposhnikoviae） and mahuang （Herba Ephedrae） for diffusing the lung， dispersing wind， and consolidating defensive qi. For yang deficiency with loss of regulation pattern， wind medicinals are employed to elevate yang and assist transformation， such as shengma （Rhizoma Cimicifugae） and gegen （Radix Puerariae Lobatae） for raising clear yang， warming and activating the spleen and kidney. For binding of turbidity and stasis pattern， wind medicinals with scurrying and collateral‑unblocking properties are used， such as jixueteng （Caulis Spatholobi）， luoshiteng （Caulis Trachelospermi）， and chuanshanlong （Rhizoma Dioscoreae Nipponicae） for dispelling wind， activating blood， resolving stasis， and directing turbidity downward. In all these methods， the core principle is to use wind medicinals to regulate qi movement， open and unblock the sweat pores， and separately eliminate turbid pathogens， thereby providing a theoretical and practical basis for the traditional Chinese medicine diagnosis and treatment of RNS in children.

Based on the theory of "cold qi generates turbidity" described in the Inner Canon of Yellow Emperor （《黄帝内经》）， together with the physiological characteristics of children， who are considered to have an inherent insufficiency of the lung， spleen， and kidney， and the clinical features of recurrent refractory nephrotic syndrome （RNS）， this article proposes that the pathogenesis of RNS in children is characterized by yang deficiency with internal cold， turbidity arising from cold， latent turbidity transforming into toxin， activation by newly contracted pathogens， and turbid toxins damaging the collaterals. The core pathogenesis is identified as yang deficiency， turbidity coagulation， and collateral damage. Accordingly， the general treatment principle is warming yang and eliminating turbidity， with coordination of three methods including warming yang to strengthen the body's foundation， promoting yang to relieve constraint， and raising yang while replenishing qi. Zhenwu Decoction （真武汤） is employed as the basic prescription with modification according to syndrome differentiation， to achieve an effect eliminating turbidity and arresting leakage， restoring kidney function by unblocking the collaterals， and consolidating recovery to prevent relapse.

Background: Maturity-onset diabetes of the young (MODY) due to variants of hepatocyte nuclear factor 1-beta (HNF1β) (MODY5) has not been well studied in the Chinese population. This study aimed to estimate its prevalence and evaluate the application of a clinical screening method (Faguer score) in Chinese early-onset diabetes (EOD) patients. Methods: Among 679 EOD patients clinically diagnosed with type 2 diabetes mellitus (age at diagnosis ≤40 years), the exons of HNF1β were sequenced. Functional impact of rare variants was evaluated using a dual-luciferase reporter system. Faguer scores ≥8 prompted multiplex ligation-dependent probe amplification (MLPA) for large deletions. Pathogenicity of HNF1β variants was assessed following the American College of Medical Genetics and Genomics (ACMG) guidelines. Results: Two rare HNF1β missense mutations (E105K and G454R) were identified by sequencing in five patients, showing functional impact in vitro. Another patient was found to have a whole-gene deletion by MLPA in 22 patients with the Faguer score above 8. Following ACMG guidelines, six patients carrying pathogenic or likely pathogenic variant were diagnosed with MODY5. The estimated prevalence of MODY5 in Chinese EOD patients was approximately 0.9% or higher. Conclusion MODY5 is not uncommon in China. The Faguer score is helpful in deciding whether to perform MLPA analysis on patients with negative sequencing results.

This paper reports a case of disseminated intravascular coagulation(DIC) that occurred early after hybrid surgery for type B aortic dissection with an aortic arch aneurysm. Through analyzing the clinical manifestations, imaging findings, and treatment response of the patient, we propose that massive false-lumen thrombosis may serve as a critical trigger for early postoperative coagulation activation leading to DIC. Corresponding treatment strategies are suggested to enhance clinicians' ability to recognize and manage this critical condition.

This paper summarizes Professor SHI Zaixiang's clinical experience in treating high fever caused by sepsis using Chaihu Guizhi Ganjiang Decoction （柴胡桂枝干姜汤）. He holds that the key pathogenesis of sepsis involves constrained heat in the shaoyang and internal accumulation of water and fluids. The clinical manifestations such as high fever， chills， and alternating sensations of cold and heat are attributed to pathogenic heat constrained in the shaoyang. Meanwhile， soft tissue edema and serous cavity effusions are due to shaoyang dysfunction and internal water retention. In clinical practice， treating sepsis-related high fever requires addressing both the shaoyang-constrained heat and the associated edema and effusions. The therapeutic approach focuses on harmonizing the shaoyang and resolving internal fluids， using Chaihu Guizhi Ganjiang Decoction as the base formula with flexible modifications. Professor SHI emphasizes that this formula shows a rapid antipyretic effect， particularly in cases where multiple anti-infective treatments have failed.

Objective:To investigate the efficacy and mechanism of botulinum toxin type A (BTX-A) combined with static progressive stretching (SPS) in the treatment of traumatic knee stiffness in rats.Methods:Forty healthy male SD rats aged 8 weeks and weighing 220-300 g, were randomly divided into blank control group ( n=8) and model groups ( n=28) (including injury group, BTX-A group, SPS group and BTX-A+SPS group, with 7 in each group). Hlidebrand′s method was used to construct a traumatic knee stiffness model, with the following main steps: destruction of the joint capsule, Kirschner wire fixation, joint drilling, and removal of the internal fixation at 4 weeks. The blank control group did not receive any treatment and could move freely in the cage. The injury group moved freely after successful modeling. On the day of internal fixation removal, BTX-A was injected into the joint cavity in group BTX-A, SPS treatment was started in the SPS group, BTX-A was injected into the joint cavity and SPS treatment was started in the BTX-A+SPS group. The treatments lasted 16 days. The range of motion (ROM) and joint stiffness were measured before treatment and at 16 days after treatment. At 16 days after treatment, knee joint tissue was collected and the rats were sacrificed, and the articular capsule fibrous tissue proliferation was observed by HE and Masson staining. The expression levels of phosphorylated (p)-Smad2, Smad2, p-Smad3, Smad3, Smad4, transforming growth factor-β1 (TGF-β1), collagen type I, collagen type III, and α-smooth actin (α-SMA) were determined by Western blot. The ratio of phosphorylated protein to total protein was calculated to reflect the phosphorylation level. Results:(1) ROM: Before treatment, the ROM in the blank control group was significantly higher than that in the other groups ( P<0.05), with no significant difference in ROM among the other groups ( P>0.05). At 16 days after treatment, ROM in the injury group, BTX-A group, SPS group, and BTX-A+SPS group was lower than that in the blank control group ( P<0.05), among which ROM in the BTX-A+SPS group was significantly higher than that in the injury group, BTX-A group, and SPS group ( P<0.05). At 16 days after treatment, there was no significant difference in ROM before and after treatment in the blank control group ( P>0.05), and ROM in the other groups was significantly increased compared with that before treatment ( P<0.01). (2) Joint stiffness: At 16 days after treatment, the joint stiffness levels in the injury group, the BTX-A group, and the SPS group were (0.95±0.24)N·cm/°, (0.86±0.22)N·cm/°, and (0.65±0.09)N·cm/° respectively, which were significantly lower than (0.36±0.03)N·cm/° in the blank control group ( P<0.05). The joint stiffness level of the BTX-A+SPS group was (0.49±0.04)N·cm/°, which was not significantly different from that in the blank control group ( P>0.05), but was significantly lower than those in the injury group, BTX-A group, and SPS group ( P<0.05). (3) Fibrous tissue proliferation: at 16 days after treatment, the joint capsular structure in the blank control group was complete and clear, the fibers were arranged in order, and there was no obvious fibrous tissue proliferation. The pathological changes in the injury group were the most serious, with a large number of synovial fibrous tissue proliferation, significantly increased blood vessels in the tissue, and inflammatory cell infiltration. Compared with the SPS group and BTX-A group, the lesions in BTX-A+SPS group were milder, with only slight increase in the number of synovial cells but no obvious vascular proliferation or lymphocytes, and the overall lesions were the least severe. (4) Protein expression: the ratios of p-Smad2/Smad2 in the injury group, BTX-A group and SPS group were 1.552±0.234, 1.328±0.272 and 1.194±0.277 respectively, which were higher than 0.794±0.082 in the blank control group ( P<0.05). The ratio of p-Smad2/Smad2 in the BTX-A+SPS group was 1.013±0.123, which was not significantly different from those in the blank control group, BTX-A group or SPS group ( P>0.05), but was lower than that in the injury group ( P<0.05). At 16 days after treatment, the p-Smad3/Smad3 ratios in the injury group, BTX-A group, SPS group and BTX-A+SPS group were 2.272±0.309, 1.664±0.285, 1.381±0.276 and 1.003±0.060 respectively, which were higher than 0.515±0.051 in the blank control group ( P<0.05). The p-Smad3/Smad3 ratio in the BTX-A+SPS group was significantly lower than those in the injury group, BTX-A group and SPS group ( P<0.05). At 16 days after treatment, the level of Smad4 in the injury group (1.001±0.015) was higher than 0.294±0.076 in the blank control group ( P<0.05). However, there was no significant difference between the BTX-A group (0.664±0.051), SPS group (0.833±0.045), BTX-A+SPS group (0.467±0.068) or the blank control group ( P>0.05). The level of Smad4 in the BTX-A+SPS group was significantly lower than those in the injury group, BTX-A group and SPS group ( P<0.05). At 16 days after treatment, the level of TGF-β1 in the injury group (1.004±0.407) was higher than 0.269±0.122 in the blank control group ( P<0.05), while there was no significant difference between the BTX-A group (0.564±0.194), SPS group (0.422±0.086) and BTX-A+SPS group (0.347±0.161) and the blank control group ( P>0.05). The level of TGF-β1 in the BTX-A+SPS group was significantly lower than those in the injury group, BTX-A group and SPS group ( P<0.05). At 16 days after treatment, the level of type I collagen in the injury group was 0.999±0.170, higher than 0.299±0.139 in the blank control group ( P<0.05), while there was no significant difference between the BTX-A group (0.542±0.278), SPS group (0.561±0.165), and BTX-A+SPS group (0.537±0.045) and the blank control group ( P>0.05). The level of collagen type I in the BTX-A+SPS group was significantly lower than those in the injury group, BTX-A group, and SPS group ( P<0.05). At 16 days after treatment, the level of type III collagen in the injury group was 1.002±0.126, higher than 0.239±0.106 in the blank control group ( P<0.05), while there was no significant difference between the BTX-A group (0.661±0.062), SPS group (0.595±0.062), and BTX-A+SPS group (0.504±0.269) and the blank control group ( P>0.05). The level of collagen type III in the BTX-A+SPS group was significantly lower than those in the injury group, BTX-A group, and SPS group ( P<0.05). At 16 days after treatment, the level of α-SMA in the injury group was 0.998±0.074, higher than 0.130±0.023 in the blank control group ( P<0.05), while there was no significant difference between the BTX-A group (0.358±0.060), SPS group (0.432±0.230), and BTX-A+SPS group (0.293±0.135) and the blank control group ( P>0.05). The level of α-SMA in the BTX-A+SPS group was significantly lower than those in the injury group, BTX-A group and SPS group ( P<0.05). Conclusions:Compared with single treatment, the combination of BTX-A and SPS demonstrates significantly greater efficacy in the treatment of traumatic knee stiffness in rats. This combined approach not only enhances joint mobility and elasticity but also effectively inhibits joint capsule fibrosis. The underlying mechanism may involve the further suppression of TGF-β1 expression in the joint capsule, leading to reduced phosphorylation levels of Smad2 and Smad3. This, in turn, inhibits the binding of Smad2 and Smad3 to the Smad4 receptor, ultimately downregulating the expression of the downstream proteins of the TGF-β/Smad signaling pathway, such as collagen type I, collagen type III and α-SMA.