ObjectiveTo observe the effect of heat-sensitive moxibustion on quality of life and immune function in non-small cell lung cancer （NSCLC） patients undergoing chemotherapy. MethodsSeventy NSCLC patients with qi deficiency and phlegm stasis syndrome were randomly divided into an intervention group and a control group， with 35 cases in each group. The control group received chemotherapy combined with routine symptomatic treatment， while the intervention group additionally received heat-sensitive moxibustion since the first day of chemotherapy. Acupoints included Dazhui （GV14）， bilateral Feishu （BL13）， Zhongwan （CV12）， Qihai （CV6）， and Guanyuan （CV4）. The site exhibiting the strongest heat-sensitization response was selected for moxibustion. Treatment was administered for 45 minutes per session， three times weekly for three consecutive weeks， totaling nine sessions. Before and after treatment， quality of life was assessed using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire （EORTC QLQ-C30）， and traditional Chinese medicine （TCM） syndrome scores were evaluated. Peripheral blood levels of natural killer （NK） cells and T-lymphocyte subsets including CD3⁺， CD4⁺， and CD8⁺， and CD4⁺/CD8⁺ ratio were measured. Levels of programmed cell death protein-1 （PD-1）， including PD-1⁺CD4⁺ and PD-1⁺CD8⁺ cells， were also assessed. Liver and renal function were monitored before and after treatment， and adverse events were recorded. ResultsIn the intervention group， 1 participant withdrew and 1 was excluded， while in the control group， 2 participants withdrew. Ultimately， 33 participants in each group were included in the final analysis. The intervention group showed significant improvements in physical， role， emotional， cognitive， and social functioning， as well as global health status after treatment， while scores for fatigue， nausea and vomiting， dyspnea， appetite loss， diarrhea， and TCM syndrome scale were significantly decreased （P＜0.05）. Moreover， the intervention group demonstrated higher scores in physical functioning， role functioning， and global health status， as well as lower scores for fatigue， nausea and vomiting， dyspnea， appetite loss， diarrhea， and the TCM syndrome scale than the control group （P＜0.05）. After treatment， the levels of peripheral NK cells and PD-1⁺CD8⁺ T cells in the intervention group increased significantly； furthermore， the intervention group exhibited higher peripheral NK cell levels and lower PD-1⁺CD8⁺ T cell levels than the control group （P＜0.05）. No significant differences were found in liver or renal function between the two groups （P＞0.05）. In addition， no adverse events such as burns or moxibustion-induced syncope occurred during the study. ConclusionHeat-sensitive moxibustion as an adjunctive therapy may enhance immune function， alleviate clinical symptoms， and improve quality of life， while demonstrating a favorable safety profile in NSCLC patients with qi deficiency and phlegm stasis.

ObjectiveFlavonoids are clinically significant natural products, yet their oxygen-glycosylation in aqueous environments relies heavily on expensive nucleotide-activated sugar donors such as UDP-glucose. Liquid-liquid phase separation (LLPS) creates specialized, membraneless physicochemical microenvironments capable of modulating enzymatic functions and overcoming mass transfer limitations. This study aims to investigate whether the gut microbiota-derived DgpB/C complex—a multienzyme system traditionally recognized for cleaving stable C-glycosidic bonds and facilitating isomerization—can undergo functional remodeling within phase-separated condensates. Our core objective is to elucidate the role of phase separation in expanding enzymatic catalytic plasticity and to provide a non-canonical, highly cost-effective biocatalytic mechanism for the direct utilization of free sugars in the synthesis of O-glycosylated natural products. MethodsAn artificial phase-separation platform was constructed utilizing the multivalent arginine-glycine-glycine motif (RGG)-repeat domain derived from the Caenorhabditis elegans LAF-1 protein. To ensure precise spatial compartmentalization, the DgpB/C complex was specifically recruited into the RGG condensates via a high-affinity SZ1/SZ2 heterodimerization tag system. Condensate formation and substrate partitioning were visualized using light and confocal fluorescence microscopy. The chemical structures and regioselectivity of the reaction products were rigorously characterized using high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometry (LC-MS)/MS systems. Furthermore, molecular docking and 20-ns molecular dynamics (MD) simulations were performed via the Hermite platform and Uni-GBSA pipeline to elucidate the structural and thermodynamic basis underlying the phase-transition-induced functional shift. ResultsWe observed that the condensates formed by RGG proteins selectively recruited and significantly enriched hydrophobic flavonoid substrates. Strikingly, within the LLPS microenvironment, the DgpB/C complex—which typically exhibits only degradative or isomerase activities—underwent a profound functional remodeling, transforming into an efficientO-glycosyltransferase. Diverging from canonical pathways that require high-energy donors, the sequestered DgpB/C complex directly utilized unactivated free glucose to catalyze the formation of new O-glycosidic bonds. This remodeled activity was found to be evolutionarily conserved across DgpB/C homologs from diverse gut microbiota strains, such as P581a and W974-1. LC-MS/MS analysis further revealed that the phase-separated environment reduced the regioselectivity constraints of the enzyme, enabling catalytic action on multiple hydroxyl positions of the flavonoid scaffold. MD simulations further indicated that the low-water-activity microenvironment of the condensates reconfigured the conformational dynamics of the catalytic pocket, favoring a spatial orientation highly conducive to dehydration condensation. ConclusionThis study demonstrates that LLPS drives the functional remodeling of the gut microbiota enzyme DgpB/C through the reconfiguration of the physicochemical microenvironment. These findings challenge traditional perceptions regarding the functional boundaries of metabolic enzymes and reveal a novel biocatalytic pathway that bypasses the requirement for nucleotide-activated sugars. Consequently, this provides a highly promising artificial compartmentalization strategy for the green manufacturing of complex, high-value-added natural products.

ObjectiveTo investigate the effects and underlying mechanisms of Modified Yupingfeng Nasal Spray （玉屏风加味鼻喷剂， MYNS） on nasal mucosal tissue remodeling in allergic rhinitis （AR） model rats based on the Janus kinase 2 （JAK2）/ signal transducer and activator of transcription 3 （STAT3） signaling pathway. MethodsThe chemical constituents of MYNS were identified and analyzed using liquid chromatography-tandem mass spectrometry （LC-MS/MS）. Network pharmacology and molecular docking were integrated to identify the potential targets and signaling pathways of MYNS in the treatment of AR， and to verify the crucial role of the JAK2/STAT3 pathway. Forty rats were randomly divided into blank group， model group， MYNS group， and mometasone furoate nasal spray group， with 10 rats per group. Except for the blank group， the AR rat model was established by ovalbumin （OVA） induction. After successful modeling， rats in the MYNS group received an intranasal instillation of 50 μl of MYNS at concentration of 1.05 g·ml^-¹ in each nostril， while the mometasone furoate nasal spray group received 50 μl of corresponding spray per nostril， and the model group received 50 μl of normal saline per nostril. Treatments were administered once daily. After 14 consecutive days of intervention， the frequencies of nosal scratching and sneezing in rats within 15 minutes were recorded. Hematoxylin-eosin （HE） staining was used to assess morphological changes in the nasal mucosa and perform pathological scoring. Masson staining was used to evaluate collagen fiber deposition in nasal mucosal tissue and calculate the collagen volume fraction （CVF）. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining was performed to detect apoptosis in nasal mucosal cells and record the number of apoptotic cells. Immunofluorescence assay was used to detect the expression of E-cadherin （E-Cad） in the nasal mucosa. Enzyme-linked immunosorbent assay （ELISA） was used to determine the serum levels of interleukin-4 （IL-4）， interferon-γ （IFN-γ）， histamine （HIS）， immunoglobulin E （IgE）， superoxide dismutase （SOD）， and malondialdehyde （MDA）. Transmission electron microscopy was used to observe the ultrastructure of mitochondria in nasal mucosal epithelial cells. Flow cytometry was used to measure mitochondrial membrane potential （MMP） and reactive oxygen species （ROS） levels. Western Blot was used to determine the protein expression levels of collagen Ⅲ （Collagen Ⅲ）， α-smooth muscle actin （α-SMA）， Bcl-2-associated X protein （Bax）， Caspase-3， JAK2， phosphorylated JAK2 （p-JAK2）， STAT3， and phosphorylated signal transducer and activator of transcription 3 （p-STAT3）. ResultsA total of 626 chemical constituents were identified by LC-MS/MS. Network pharmacology screening identified 450 active ingredients. Nine intersecting components and 39 drug-AR intersecting targets were obtained. KEGG enrichment analysis indicated the involvement of signaling pathways including JAK2/STAT3. The animal experimental results showed that， compared with the blank group， rats in the model group exhibited significantly increased frequencies of nasal scratching and sneezing， as well as elevated CVF and the number of apoptotic cells， while the levels of E-Cad， MMP， and serum IFN-γ and SOD significantly decreased； meanwhile， the serum levels of IL-4， IgE， HIS， ROS， and MDA， along with the protein expression levels of Collagen Ⅲ， α-SMA， Bax， Caspase-3， p-JAK2， and p-STAT3 in the nasal mucosa， significantly increased （P＜0.05）， accompanied by aggravated pathological damage in the nasal mucosa， increased collagen fiber deposition， and abnormal mitochondrial morphology. Compared to the model group， rats in the MYNS group showed improvements in all the aforementioned indicators except for HIS （P＜0.05）， and those in the mometasone furoate nasal spray group showed improvements in all indicators except for IL-4， IgE， and SOD levels （P＜0.05）. ConclusionThe mechanism of MYNS in treating AR may be related to inhibiting the activation of the JAK2/STAT3 signaling pathway， reducing inflammatory responsesand oxidative stress， ameliorating mitochondrial damage， and suppressing nasal mucosal cell apoptosis， thereby improving nasal mucosal tissue pathological remodeling.

ObjectiveTo investigate the effects and underlying mechanisms of Modified Yupingfeng Nasal Spray （玉屏风加味鼻喷剂， MYNS） on nasal mucosal tissue remodeling in allergic rhinitis （AR） model rats based on the Janus kinase 2 （JAK2）/ signal transducer and activator of transcription 3 （STAT3） signaling pathway. MethodsThe chemical constituents of MYNS were identified and analyzed using liquid chromatography-tandem mass spectrometry （LC-MS/MS）. Network pharmacology and molecular docking were integrated to identify the potential targets and signaling pathways of MYNS in the treatment of AR， and to verify the crucial role of the JAK2/STAT3 pathway. Forty rats were randomly divided into blank group， model group， MYNS group， and mometasone furoate nasal spray group， with 10 rats per group. Except for the blank group， the AR rat model was established by ovalbumin （OVA） induction. After successful modeling， rats in the MYNS group received an intranasal instillation of 50 μl of MYNS at concentration of 1.05 g·ml^-¹ in each nostril， while the mometasone furoate nasal spray group received 50 μl of corresponding spray per nostril， and the model group received 50 μl of normal saline per nostril. Treatments were administered once daily. After 14 consecutive days of intervention， the frequencies of nosal scratching and sneezing in rats within 15 minutes were recorded. Hematoxylin-eosin （HE） staining was used to assess morphological changes in the nasal mucosa and perform pathological scoring. Masson staining was used to evaluate collagen fiber deposition in nasal mucosal tissue and calculate the collagen volume fraction （CVF）. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining was performed to detect apoptosis in nasal mucosal cells and record the number of apoptotic cells. Immunofluorescence assay was used to detect the expression of E-cadherin （E-Cad） in the nasal mucosa. Enzyme-linked immunosorbent assay （ELISA） was used to determine the serum levels of interleukin-4 （IL-4）， interferon-γ （IFN-γ）， histamine （HIS）， immunoglobulin E （IgE）， superoxide dismutase （SOD）， and malondialdehyde （MDA）. Transmission electron microscopy was used to observe the ultrastructure of mitochondria in nasal mucosal epithelial cells. Flow cytometry was used to measure mitochondrial membrane potential （MMP） and reactive oxygen species （ROS） levels. Western Blot was used to determine the protein expression levels of collagen Ⅲ （Collagen Ⅲ）， α-smooth muscle actin （α-SMA）， Bcl-2-associated X protein （Bax）， Caspase-3， JAK2， phosphorylated JAK2 （p-JAK2）， STAT3， and phosphorylated signal transducer and activator of transcription 3 （p-STAT3）. ResultsA total of 626 chemical constituents were identified by LC-MS/MS. Network pharmacology screening identified 450 active ingredients. Nine intersecting components and 39 drug-AR intersecting targets were obtained. KEGG enrichment analysis indicated the involvement of signaling pathways including JAK2/STAT3. The animal experimental results showed that， compared with the blank group， rats in the model group exhibited significantly increased frequencies of nasal scratching and sneezing， as well as elevated CVF and the number of apoptotic cells， while the levels of E-Cad， MMP， and serum IFN-γ and SOD significantly decreased； meanwhile， the serum levels of IL-4， IgE， HIS， ROS， and MDA， along with the protein expression levels of Collagen Ⅲ， α-SMA， Bax， Caspase-3， p-JAK2， and p-STAT3 in the nasal mucosa， significantly increased （P＜0.05）， accompanied by aggravated pathological damage in the nasal mucosa， increased collagen fiber deposition， and abnormal mitochondrial morphology. Compared to the model group， rats in the MYNS group showed improvements in all the aforementioned indicators except for HIS （P＜0.05）， and those in the mometasone furoate nasal spray group showed improvements in all indicators except for IL-4， IgE， and SOD levels （P＜0.05）. ConclusionThe mechanism of MYNS in treating AR may be related to inhibiting the activation of the JAK2/STAT3 signaling pathway， reducing inflammatory responsesand oxidative stress， ameliorating mitochondrial damage， and suppressing nasal mucosal cell apoptosis， thereby improving nasal mucosal tissue pathological remodeling.

The accumulation of uremic toxins such as urea nitrogen, blood creatinine, and uric acid of patients with renal failure in vivo would lead to aggravated kidney damage. In this study, coated aldehyde oxy-starch (CAO) was used as an adsorbent to investigate its in vitro adsorption performance on renal failure indexes for urea, indoxyl sulfate (INS), monomethylamine (MMA), dimethylamine (DMA), uric acid (UA), and creatinine (Cr). The effects of variables such as pH, temperature, concentration, dosage, and time on the adsorption capacity of CAO were systematically investigated, employing analytical techniques of high-performance liquid chromatography (HPLC) and gas chromatography (GC). The results revealed that CAO exhibited a strong adsorption capacity for urea, INS, and MMA, alongside a moderate adsorption capacity for DMA, UA, and Cr. The adsorption kinetics and thermodynamic studies indicated that the adsorption of urea and UA by CAO were fitted in pseudo-first-order kinetics, and the adsorption isotherm aligned with the Freundlich adsorption model. The enthalpy change ΔH of urea in adsorption was in the range of 40 to 60 kJ·mol^-1, which demonstrated the presence of strong adsorption force due to the interactions of coordinating groups. The ΔH of UA was greater than 80 kJ·mol^-1, indicating the generation of chemical bonds during the adsorption. Both of them, Gibbs free energy ΔG was less than 0, within the range of -20 to 0 kJ·mol^-1, suggested that the adsorption of urea and UA by CAO occurred spontaneously as physical adsorption process. The adsorption entropy ΔS of urea and UA was > 0, which indicated an increase in entropy throughout the adsorption. The infrared spectroscopygram showed the formation of a chemical bond, specifically the imine bond, following the adsorption of urea by CAO, thereby indicating a chemical reaction during the adsorption. This study elucidates the adsorption mechanism of CAO on various indexes of renal failure, providing a scientific basis for its clinical usage.

Objective: To develop a modified calculation formula for renal tumor volume and tumor contact surface area (CSA) based on the modeling results of 3D Slicer software, and to create a webpage of the calculation formula for use. Methods: The general information and tumor anatomical data of 98 patients who underwent partial nephrectomy during Jan.2021 and Jul.2023 in the Second Affiliated Hospital of Xi'an Jiaotong University were retrospectively analyzed.The imaging data were input into 3D Slicer software in the form of Dicom files for tumor and ipsilateral kidney modeling to obtain tumor anatomical data.The relationship between tumor anatomical parameters and tumor volume and CSA was analyzed using multifactorial linear regression.The initial modified formulas (V2, C2) and the optimized modified formulas (V3, C3) for tumor volume over CSA were established, respectively, after insignificant variables were eliminated.The mean square error (MSE) and Akaike information criterion (AIC) of the modified and traditional formulas (V1, C1) were compared, and the formula with the smallest MSE and AIC was selected as the optimal tumor volume and CSA calculation formula.The median tumor volume and CSA obtained from 3D modeling were used as the cutoff values.The optimal formula and conventional formula were applied to calculate tumor volume and CSA for all patients, and risk stratification was performed for all patients based on these cutoff values, and the perioperative indicators of patients in the upper and lower groups were compared.Finally, an online calculation tool was developed based on HTML. Results: Based on multifactorial linear regression analysis, we obtained the modified tumor volume calculation formula: V=0.382abc+2.488a+2.372b－4.146c+1.948（V2）, V=0.469abc－4.586c+13.816（V3）; the modified tumor CSA calculation formula CSA=2.469a －2.262L －19.23a+6.206b+1.212c+18.017L+1.616h－3.97h －2.185h/h －0.388（C2）, CSA=2.376a －2.144L －20.157a+5.024b+1.128c+17.578L+2.525h－2.634（C3）.Both of the modified volume formula (MSE=151.298 vs. 127.807 vs. 104.106) and modified CSA formula (MSE=309.878 vs.23.556 vs.30.388) had smaller errors compared to the conventional formula.The modified volume calculation formula showed that bleeding was more and thermal ischemia time was longer in patients with larger tumor volumes than in patients with smaller tumor volumes (P<0.05); and the modified CSA calculation formula showed that bleeding was more, surgery and thermal ischemia time were longer in patients with high CSA than in patients with low CSA (P＜0.05).Finally, V3 and C3 are selected as the best calculation formula, and a web page (https://lizihao-bot.github.io/RCC-Calculate/) was established for easy use. Conclusion: This study combined data from a medical information technology platform with numerical modeling methods to provide a faster and more accurate method to calculate the renal tumor volume and CSA.Meanwhile, a webpage version of the tool was developed to enhance its practicability.

ObjectiveTo evaluate the efficacy and safety of Xiaoji Hufei Formula in protecting children with close contact exposure to influenza， and to provide reference and evidence-based support for better clinical prevention and treatment of influenza in children. MethodsA multicenter， prospective， non-randomized， parallel， controlled trial was conducted from October 2021 to May 2022 in five hospitals， including Dongfang Hospital of Beijing University of Chinese Medicine. Confirmed influenza cases and influenza-like illness （ILI） cases were collected， and eligible children with close contact exposure to these cases were recruited in the outpatient clinics. According to whether the enrolled close contacts were willing to take Xiaoji Hufei formula for influenza prevention， they were assigned to the observation group （108 cases） or the control group （108 cases）. Follow-up visits were conducted on days 7 and 14 after enrollment. The primary outcomes were the incidence of ILI and the rate of laboratory-confirmed influenza. Secondary outcomes included traditional Chinese medicine （TCM） symptom score scale for influenza， influenza-related emergency （outpatient） visit rate， influenza hospitalization rate， and time to onset after exposure to influenza cases. ResultsA total of 216 participants were enrolled， with 108 in the observation group and 108 in the control group. Primary outcomes： （1） Incidence of ILI： The incidence was 12.0% （13/108） in the observation group and 23.1% （25/108） in the control group， with the observation group showing a significantly lower incidence （χ²=4.6， P<0.05）. （2） Influenza confirmation rate： 3.7% （4/108） in the observation group and 4.6% （5/108） in the control group， with no statistically significant difference. Secondary outcomes： （1） TCM symptom score scale： after onset， nasal congestion and runny nose scores differed significantly between the two groups （P<0.05）， while other symptoms such as fever， sore throat， and cough showed no significant differences. （2） Influenza-related emergency （outpatient） visit rate： 84.6% （11 cases） in the observation group and 96.0% （24 cases） in the control group， with no significant difference. （3） Time to onset after exposure： The median onset time after exposure to index patients was 7 days in the observation group and 4 days in the control group， with a statistically significant difference （P<0.05）. ConclusionIn previously healthy children exposed to infectious influenza cases under unprotected conditions， Xiaoji Hufei formula prophylaxis significantly reduced the incidence of ILI. Xiaoji Hufei Formula can be recommended as a specific preventive prescription for influenza in children.

BACKGROUND: Fibrosis of the connective tissue in the vaginal wall predominates in pelvic organ prolapse (POP), which is characterized by excessive fibroblast-to-myofibroblast differentiation and abnormal deposition of the extracellular matrix (ECM). Our study aimed to investigate the effect of ECM stiffness on vaginal fibroblasts and to explore the role of methyltransferase 3 (METTL3) in the development of POP. METHODS: Polyacrylamide hydrogels were applied to create an ECM microenvironment with variable stiffness to evaluate the effects of ECM stiffness on the proliferation, differentiation, and expression of ECM components in vaginal fibroblasts. METTL3 small interfering RNA and an overexpression vector were transfected into vaginal fibroblasts to evaluate the effects of METTL3 silencing and overexpression on matrix stiffness-induced vaginal fibroblast-to-myofibroblast differentiation and abnormal modulation of the ECM. Both procedures were detected by 5-ethynyl-2'-deoxyuridine (EdU) staining, Western blotting (WB), quantitative real-time polymerase chain reaction (RT-qPCR), and immunofluorescence (IF). RESULTS: Vaginal fibroblasts from POP patients exhibited increased proliferation ability, increased expression of α-smooth muscle actin (α-SMA), decreased expression of collagen I/III, and significantly decreased expression of tissue inhibitors of matrix metalloproteinases (TIMPs) in the stiff matrix ( P <0.05). Compared with those from non-POP patients, vaginal wall tissues from POP patients demonstrated a significant increase in METTL3 content ( P <0.05). However, silencing METTL3 expression in vaginal fibroblasts with high ECM stiffness resulted in decreased proliferation ability, decreased α-SMA expression, an increased ratio of collagen I/III, and increased TIMP1 and TIMP2 expression. Conversely, METTL3 overexpression significantly promoted the process of increased proliferation ability, increased α-SMA expression, decreased ratio of collagen I/III and decreased TIMP1 and TIMP2 expression in the soft matrix ( P <0.05). CONCLUSIONS Elevated ECM stiffness can promote excessive proliferation, differentiation, and abnormal ECM modulation, and the expression of METTL3 plays an important role in alleviating or aggravating matrix stiffness-induced vaginal fibroblast-to-myofibroblast differentiation and abnormal ECM modulation.
Humans ; Female ; Extracellular Matrix/metabolism* ; Cell Differentiation/genetics* ; Methyltransferases/metabolism* ; Pelvic Organ Prolapse/pathology* ; Fibroblasts/metabolism* ; Myofibroblasts/metabolism* ; Vagina/metabolism* ; Cell Proliferation/physiology* ; Cells, Cultured ; Middle Aged

Nonobstructive azoospermia (NOA), one of the most severe types of male infertility, etiology often remains unclear in most cases. Therefore, this study aimed to detect four biallelic detrimental variants (0.5%) in the minichromosome maintenance domain containing 2 ( MCMDC2 ) genes in 768 NOA patients by whole-exome sequencing (WES). Hematoxylin and eosin (H&E) demonstrated that MCMDC2 deleterious variants caused meiotic arrest in three patients (c.1360G>T, c.1956G>T, and c.685C>T) and hypospermatogenesis in one patient (c.94G>T), as further confirmed through immunofluorescence (IF) staining. The single-cell RNA sequencing data indicated that MCMDC2 was substantially expressed during spermatogenesis. The variants were confirmed as deleterious and responsible for patient infertility through bioinformatics and in vitro experimental analyses. The results revealed four MCMDC2 variants related to NOA, which contributes to the current perception of the function of MCMDC2 in male fertility and presents new perspectives on the genetic etiology of NOA.
Humans ; Male ; Azoospermia/genetics* ; Meiosis/genetics* ; Spermatogenesis/genetics* ; Adult ; Exome Sequencing ; Microtubule-Associated Proteins/genetics* ; Alleles ; Infertility, Male/genetics*

To evaluate the therapeutic effect of a modified Devine procedure with a subcutaneous sliding fixation method for the treatment of congenital concealed penis, we retrospectively selected 45 patients with congenital concealed penises who were admitted to General Hospital of Ningxia Medical University (Yinchuan, China) between September 2020 and November 2023. In all cases, the penis was observed to be short, and retracting the skin at the base revealed a normal penile body, which immediately returned to its original position upon release. All patients underwent the modified Devine procedure with subcutaneous sliding fixation and completed a 12-week postoperative follow-up. A statistically significant increase in penile length was observed postoperatively, with the median length increasing from 4.0 (interquartile range [IQR]: 3.5-4.8; 95% confidence interval [CI]: 3.9-4.4) cm to 8.0 (IQR: 7.8-8.0; 95% CI: 7.7-7.9) cm, with P < 0.001. The parents were satisfied with the outcomes, including increased penile length, improved hygiene, and enhanced esthetics. Except for mild foreskin edema in all cases, no complications (such as infections, skin necrosis, or penile retraction) were observed. The edema was resolved within 4 weeks after the operation. This study demonstrates that the modified Devine procedure utilizing the subcutaneous sliding fixation method yields excellent outcomes with minimal postoperative complications, reduced penile retraction, and high satisfaction rates among patients and their families.
Humans ; Male ; Penis/abnormalities* ; Retrospective Studies ; Urologic Surgical Procedures, Male/methods* ; Treatment Outcome ; Child ; Plastic Surgery Procedures/methods*