Minimal Inflammation Research Articles

Controlled Thermal Stimulation Using 980-nm Laser for Collagen Remodeling.

Collagen plays a key role in maintaining skin structure and function. Energy based devices such as radiofrequency and ultrasound stimulate collagen synthesis through thermal stimulation, but lack precise temperature regulation. This study evaluated collagen synthesis induced by controlled thermal stimulation using a 980 nm laser. An exvivo test identified conditions to achieve 50°C-60°C. Based on these results, 2.5 W laser irradiation for 35 s was applied to invivo rat skin. Skin samples were collected on days 0, 14, and 28. Histology showed a three-fold increase in dermal thickness and a 15% increase in collagen density at day 28. RT-qPCR confirmed upregulation of FGF2, AKT, and COL3A1, with no significant changes in IL-1β or IL-6, and decreased NF-κB expression, indicating minimal inflammation. These findings demonstrate that controlled 980 nm laser stimulation enhances collagen synthesis without damaging skin tissue. Future studies will assess thermal distribution using fiber Bragg grating sensors.

Remote-Controlled Magnetic Stimulation of Cell-Based Bioengineered Tissues for In Situ Bone Regeneration.

The native cell microenvironment activates signaling pathways through mechanotransduction mechanisms, influencing cells' physiological and functional outcomes. Magnetic fields are explored to manipulate these environments, and magnetic nanoparticles (MNPs) are highlighted as nano-instructive agents capable of activating key signaling pathways, presenting exciting possibilities in tissue engineering. Still, the ability to precisely control the assembly and differentiation of stem cells within a dynamically responsive microenvironment, crucial for effective tissue regeneration, remains unexplored. This study showcases a novel method wherein MNPs facilitate the precise assembly of magnetically responsive cells into complex 3D tissue structures upon internalization and exposure to temporally defined cyclic magnetic fields. By remotely stimulating these constructs, it is demonstrated for the first time the possibility of remote-controlled modulation of stem cell fate in vivo without biochemical supplementation. Notably, this approach led to ectopic bone formation, highlighting the ability of magnetic actuation to drive osteogenesis in non-bone environments. MNP-driven mechanical stimulation of implanted tissues functions as a bioresponsive system guiding osteogenic differentiation of human adipose-derived stem cells. The in vivo model further illustrates accelerated construct integration, enhanced osteogenic differentiation, and minimal local inflammation, underscoring the potential of this less invasive, remotely controllable platform to advance regenerative strategies for bone engineering.

Gall bladder agenesis and ductal plate malformation in an adult Rottweiler

Abstract Gall bladder agenesis and ductal plate malformation (DPM) are rarely diagnosed hepatobiliary anomalies in dogs. This case report documents the clinical findings, diagnostic test results and outcome in a 3.5‐year‐old female Rottweiler with gall bladder agenesis associated with DPM. The dog was presented with a 2‐week history of diarrhoea and vomiting. Biochemical test results were consistent with hepatopathy. Abdominal ultrasound revealed absence of a gall bladder, ascites and asymmetrically small liver lobes with irregular contours and a heterogeneous but overall increased echogenicity. Explorative laparotomy confirmed the absence of a gall bladder and small‐sized liver lobes with a very irregular surface and firm consistency. Histological examination of liver biopsies showed severe portal‐to‐portal bridging fibrosis, tortuous and multifocally ectatic bile duct profiles, multifocal absence of portal veins, increased arteriolar profiles, direct intersection of bile ducts with hepatocytes and lymphangiectasia with minimal periportal inflammation, consistent with DPM. The dog developed hepatic encephalopathy and was euthanased.

Mitochondrial Dysfunction in Systemic Sclerosis

ObjectivesSystemic sclerosis (SSc) is a chronic inflammatory and fibrotic disease with the involvement of skin at its onset. Although numerous pathogenic processes contribute to SSc, its root cause remains poorly understood. We hypothesize that valuable insights into SSc pathogenesis can be gained by characterizing interactions between functional niches within the skin from SSc patients using spatial transcriptomics. We aimed to: 1. To identify and map functional zones in SSc skin based on their cellular composition and patterns of mRNA expression. 2. To objectively designate dominant molecular signatures and pathways to those discrete dermal zones using bioinformatic tools.MethodsSkin biopsies from 11 patients with limited and diffuse cutaneous SSc were analyzed using spatial transcriptomic sequencing. Single-cell RNA sequencing (scRNA-seq)[1] were used to deconvolve dermal cell types. Sequencing reads were processed using Space Ranger and Cell Ranger pipelines. Clustering spatial and single-cell data was performed with Seurat. Identified clusters were annotated by differentially expressed genes, with functional enrichment analysis conducted using GO and KEGG pipelines via ClusterProfiler.ResultsSpatial transcriptomic analysis identified 6 distinct transcriptomic clusters spanning the dermis in an interwoven pattern not aligned with the histological layers of the skin. We focused on 3 major dermal clusters (designated as clusters 0, 1, and 4) comprising >90% of the dermal area. Cluster 0 was heterogeneous with respect to cell types, included inflammatory signature, and was functionally dominated by mitochondrial metabolic pathways. Cluster 1 contained mostly fibroblasts exhibiting fibrotic pathways with minimal inflammation. Cluster 4 represented perivascular areas with prominent smooth muscle cells and myofibroblast signatures. The mitochondrial gene dysregulation in cluster 0 showed downregulation of nuclear DNA-encoded mitochondrial genes and upregulation of mitochondrial DNA-encoded genes, indicating stress-adaptation mechanisms in this functional zone. In contrast, Cluster 1 exhibited downregulation of both nuclear and mitochondrial genes - suggesting complete collapse of mitochondrial function (Figure).ConclusionFor the first time, we revealed discrete zones in SSc skin characterized by inflammation accompanied by mitochondrial stress, separated from the areas of fibrosis where the mitochondrial function was disintegrated. Our study supports previous research indicating that dysregulated mitochondria are central, if not fundamental, to the pathogenesis of SSc. [1.] Tabib T. Nat Commun 2021;12:4384.

Histological and Histomorphometric Insights into Implant Bed Preparation: A Systematic Review.

Objective: To assess the bone histological changes and histomorphometric parameters when using different implant site preparation methods. Methods: A systematic search was conducted in March 2025 across the PubMed, Scopus, and Web of Science (WoS) databases following the PRISMA guidelines. An initial search of the databases yielded 338 potentially relevant articles. Ultimately, a total of 29 articles were included in the qualitative synthesis in this review. The considerable heterogeneity among the included studies precluded a meta-analysis. Results: This systematic review showed that, among all the assessed implant site preparation methods, which were drilling, laser, piezoelectric surgery, osteotomy and osteodensification, the classical drilling method was more likely to cause adverse changes at the drill site, such as microcracks, uneven bone margins, osteocyte damage and thermal injury. In contrast, alternative methods resulted in fewer microcracks, minimal inflammation, a reduced risk of thermal tissue damage and denser, more regular bone formation. When using these methods, the %BIC parameter was higher than when using the drilling method. Conclusions: Using alternative techniques to prepare the implant bed creates favourable conditions for proper healing and osseointegration by eliminating defects resulting from the drilling method. However, it should be noted that satisfactory results can be achieved using the classical method if the correct parameters of the drill rotation, cooling and load are employed. Further studies based on a uniform methodology are necessary to determine the most efficient and safest parameters for each method.

Invasive Aspergillosis with Intracranial Extension Initially Misdiagnosed as a Granulomatous Disease: A Case Report

Background: Invasive aspergillosis with orbital apex and intracranial involvement is rare and often misdiagnosed due to nonspecific imaging findings. Misinterpretation may lead to inappropriate therapies, such as corticosteroids, which can exacerbate fungal infections. Case Presentation: A 50-year-old immunocompetent woman with diabetes mellitus presented with right ptosis and systemic malaise. Magnetic resonance imaging (MRI) performed three months prior had shown a subtle low-signal lesion in the right orbital apex. The lesion was small and thought to represent a granulomatous process, with minimal systemic inflammation and only mild surrounding changes on imaging. Biopsy was considered too invasive at that stage, and the patient was placed under observation. Over time, her condition progressed, and repeat imaging revealed intracranial extension, including involvement of the cavernous sinus and frontal lobe. Differential diagnoses included granulomatous diseases such as sarcoidosis or tuberculosis, prompting empirical anti-tuberculosis treatment. However, the patient’s condition worsened, and biopsy of the sphenoid sinus revealed septated fungal hyphae consistent with Aspergillus species on Grocott staining. Voriconazole therapy was initiated, resulting in significant clinical and radiological improvement. Discussion: This case highlights the diagnostic challenge of identifying orbital apex aspergillosis with early MRI changes and demonstrates the risk of misdiagnosis as granulomatous disease. Differentiating fungal infections from other inflammatory etiologies based on subtle imaging features is critical, especially when considering immunosuppressive therapy. Conclusion: Clinicians should maintain a high index of suspicion for fungal infections in patients with progressive orbital apex lesions, even in the absence of classic immunosuppression. Early imaging review and biopsy are essential to prevent misdiagnosis and inappropriate treatment.

Therapeutic potential of repaglinide-embedded chitosan hydrogel in promoting wound healing.

Therapeutic potential of repaglinide-embedded chitosan hydrogel in promoting wound healing.

RELATING TRANSCRIPTOMIC PROFILES OF HUMAN LUPUS NEPHRITIS AND GLOMERULONEPHRITIS IN LUPUS-PRONE MICE

PV011 / #383Poster Topic:AS02 - Animal ModelsBackground/PurposeThe presentation of lupus nephritis (LN) is heterogeneous, but is thought to initiate with immune complex deposition in the kidney and acute inflammation that develops into a chronic condition resulting in end-stage renal disease. We sought to better understand the molecular features of LN through gene expression profiling of human disease and its relationship to that of a well-defined murine model of LN.MethodsHuman subjects were control (CTL) patients without kidney pathology and patients with ISN/RPI class II-V LN. The NZM2328 lupus-prone mouse, an established model of human LN that progresses from predisease (CTL) to acute (AGN), transitional (TGN) and chronic (CGN) nephritis, was also assessed.[1] Gene expression was analyzed from glomerular (Glom) and tubulo-interstitial (TI) regions for enrichment of informative gene modules by Gene Set Variation Analysis (GSVA).ResultsGSVA and unsupervised k-means clustering identified 4 subsets of LN in the human Glom and TI, which were ordered from least to most severe based on abnormalities in molecular profile as compared to CTL subjects. In the Glom, subset specific changes in metabolism, kidney tissue, immune, endothelial cell and podocyte modules were noted (Figure 1a). Mouse orthologs of the human gene modules were applied to analysis of the Glom from lupus-prone mice (Figure 1b). In the mouse Glom, progression from CTL to AGN and TGN was accompanied by an increase in immune/inflammatory modules and decreases in metabolism and tissue modules. CGN mice were divided between Subsets 2-4 with some mice that exhibited an inflammatory profile and others that were de-enriched for all modules indicative of a post-inflammatory state. Analysis of the human and mouse TI revealed progressive abnormalities (Figure 2). The TI samples from human CTL patients were clustered in Subset 1 and exhibited minimal immune module enrichment, whereas metabolism and kidney tubule modules were prominent (Figure 2a). Subsets 2-3 had increased of immune and decreased metabolism and kidney tubule modules. Subset 4 had minimal inflammation, but decreased kidney tubule expression. The progression of disease severity in the TI of lupus-prone mice from predisease to chronic disease was highly aligned with the molecular subset of each mouse and consistent with changes in human disease (Figure 2b).Figure 1:Clustering of GSVA enrichment scores from human and mouse lupus kidney glomeruli. (a) GSVA heatmap of kidney glomeruli from human CTL and LN patients (GSE32591) with ISN/RPI classification for enrichment of immune, metabolism, and kidney tissue gene modules. (b) GSVA heatmap of kidney glomeruli from NZM2328 mice (GSE206806) with predefined disease stage annotation for enrichment of mouse orthologs of the modules in (a).Figure 2:Clustering of GSVA enrichment scores from human and mouse lupus kidney tubulo-interstitial tissue. (a) GSVA heatmaps of kidney tubulointerstitium from human (a) NZM2328 mice (b) as in Figure 1.ConclusionsHuman and mouse LN transcriptomic profiles were strikingly similar, such that the progression in human could be related to that of murine LN. Class II patients resembled CTL and AGN mice. Class III patients were akin to AGN and TGN mice. Class IV-V patients shared profiles of TGN and some CGN mice. Alignment of the transcriptomic profiles of human and mouse LN provides new evidence on the nature of progression of human disease and also confirms the utility of the NZM2328 model of LN in defining the molecular pathogenesis of human LN.

Management of immune-tolerant chronic hepatitis B.

The immune-tolerant (IT) phase of chronic hepatitis B is a distinct stage of infection, characterized by high HBV replication, normal ALT levels, and minimal liver inflammation. Despite its classification as a benign phase, growing evidence challenges this notion, revealing immune activation, HBV DNA integration, and potential oncogenic processes even in the absence of elevated ALT. The IT phase's prolonged high viral replication raises concerns about its implications for HCC risk. Histological studies show that significant inflammation and fibrosis may exist in patients meeting IT criteria, suggesting that the current definitions may underestimate disease activity. Treatment during the IT phase remains controversial, with international guidelines largely recommending against antiviral therapy due to its limited efficacy and potential risks. However, subsets of IT patients may benefit from early intervention. The risks and benefits of therapy in IT chronic hepatitis B are not fully understood, and the lack of consensus regarding treatment thresholds further complicates clinical decision-making. This review highlights the importance of redefining IT chronic hepatitis B to include virological and histological parameters and calls for long-term studies to clarify the role of therapy in reducing fibrosis progression and HCC risk. A more precise understanding of the IT phase is essential to balance the risks of treatment against its potential benefits and to inform future therapeutic strategies.

Improved Diabetic Wound Healing via Flower Extracellular Vesicles and Carbon-Dot-Infused Alginate-Polyethylenimine Antibacterial Hydrogel.

Diabetic wounds lead to substantial challenges in healthcare systems due to prolonged healing and susceptibility to debilitating bacterial infections. Traditional wound dressings, designed to regenerate wound voids and aid healing, often lack antibacterial properties. In this study, we present a syringe-injectable hydrogel (HG) infused with rose-petal-derived extracellular vesicles (REVs) and fluorescent carbon dots (CDs), which exhibit intrinsic antibacterial activity. The HG matrix was created by combining oxidized sodium alginate (OA) with branched polyethylenimine (PEI). This formulation selectively targets Gram-negative bacteria through strong physical and mechanical interactions while preserving human erythrocytes, as confirmed by hemolytic assays. Using a Wistar rat type 1 diabetic model, we demonstrated that the HG effectively eradicates E. coli at the application site, ensuring slow release and retention of REVs and CDs at the wound site, causing minimal inflammation. REV-CD-HG represents a scalable, cost-efficient, and innovative wound dressing with promising clinical applications.

Olmesartan-associated gastroduodenitis that was detected on endoscopic follow-up

Abstract We present a rare case of olmesartan-associated gastroduodenitis in a 65-year-old female with predominant upper gastrointestinal symptoms and significant changes in endoscopic findings over a short period. The patient presented with epigastralgia and nausea but no diarrhea. Esophagogastroduodenoscopy (EGD) performed 26 months earlier showed a duodenal ulcer and partial mucosal atrophy in the lower gastric body. EGD conducted at our hospital revealed diffuse atrophic mucosa throughout the stomach and fragile mucosa from the middle gastric body to the antrum, with white purulent adhesions. Diffuse inflammatory changes were also observed in the duodenal bulb and descending part. Mucosal biopsy showed atrophic changes, inflammatory cell infiltrations, and epithelial detachments in both the stomach and duodenum. Colonoscopy findings were normal. After discontinuing olmesartan, the patient’s symptoms improved immediately. A follow-up EGD conducted 4 months after discontinuation revealed marked improvement in the stomach and duodenum. At 16 months post-discontinuation, the patient remained asymptomatic, with minimal inflammation and residual gastric atrophy observed on EGD. This case underscores the importance of considering olmesartan as a potential cause of gastroduodenitis, particularly when symptoms and endoscopic findings improve after discontinuation of the medication.

Comparative assessment of cyanoacrylate adhesive and sutures for closing donor sites of the hard palate mucosa during a single surgical procedure: a clinical case

Introduction: Suturing is still the most common wound closure method in dentistry. However, this approach has a number of drawbacks, including the risk of inflammation, delayed healing, and inconveniences for patients, necessitating the research of alternative techniques. Because of their quick polymerization in a moist environment and good biocompatibility, cyanoacrylate adhesives are considered a promising alternative option. Case description: Two donor sites of the hard palate mucosa were closed during a single surgical procedure: one using “Sulfacrylate” cyanoacrylate adhesive and the other by suturing. Clinical assessment and photo documentation were performed, and the patient’s subjective perception was analyzed 7 days and 1.5 years after surgery to compare the healing of the hard palate mucosa with different wound closure approaches. The site where the adhesive was applied showed faster healing, minimal inflammation, and excellent esthetic results without scarring. The procedure time for the adhesive was significantly shorter than for suturing. The patient reported less discomfort on the side where the adhesive was applied. Conclusion: “Sulfacrylate” cyanoacrylate adhesive is an effective and safe alternative to conventional suturing, with improved healing and comfort for patients. Further real-world studies of this approach are recommended.

FlexiPlasma Microcatheter-Embolic Material (FPM-EM) Platform: A Non-Inflammatory Pyroptosis Strategy for Precision Hepatocellular Carcinoma Therapy.

Hepatocellular carcinoma (HCC) remains a global challenge, with conventional locoregional therapies like transarterial chemoembolization (TACE) lacking tumor specificity and promoting metastasis and inflammation. Cold atmospheric plasma (CAP) offers a tumor-selective ablation strategy but suffers from limited tissue penetration. To overcome this, the FlexiPlasma microcatheter (FPM) is developed, integrating flexible non-metallic microtubes and ring-shaped electrodes for precise CAP delivery to deep tumors. The optimized FPM-generated CAP eliminates cytotoxic UV and ozone while inducing tumor-specific pyroptosis via a ROS/Caspase-8/GSDMC pathway. Gasdermin-C (GSDMC) is highly expressed in liver tumors but absent in normal tissues, ensuring selective targeting with minimal inflammation. FPM is combined with embolic material (EM), PPP@CD hydrogel, enhancing injectability, tumor embolization, and sustained drug release. This FPM-EM strategy potentiates antitumor immunity, particularly CD4+ and CD8+ T-cell responses. These findings establish FPM-EM as a safe, effective, and minimally invasive therapy for HCC, revealing a non-inflammatory pyroptosis mechanism and broadening the potential of CAP-based cancer treatments. The FPM-EM combination offers promising new therapeutic options for HCC, addressing the limitations of TACE. Furthermore, the FPM-EM platform can be extended to the interventional therapy of other tumors and adapted to incorporate various drugs and nano-/micro-materials, highlighting the strong potential for future clinical translation.

Abstract 1043: Efficacy and mechanistic insights of Shengyang Qushi Decoction in managing surufatinib-associated diarrhea

Abstract Background: Surufatinib, a novel TKI targeting VEGFRs, FGFR1, and CSF1R, treats advanced neuroendocrine tumors but often causes diarrhea, which impairs patients’ health and anti-tumor efficacy. We’ve successfully established a rat model of surufatinib-induced diarrhea. This study aims to investigate Shengyang Qushi Decoction's mechanism in treating this diarrhea, focusing on intestinal mucosal barrier and inflammation, for clinical application. Methods: Sixty male rats were randomly assigned to five groups after a 3-day acclimation period: control, model, low-dose decoction (12g/kg), high-dose decoction (24g/kg), and positive control (Loperamide 0.36mg/kg) group. Except for the control group, all received oral administration of surufatinib at a dose of 110 mg/kg, followed by corresponding treatment after 12 hours. We monitored body weight, general condition and assessed diarrhea. Histological changes in the colon were evaluated. ELISA measured plasma diamine oxidase (DAO) and D-lactate levels, as well as serum inflammatory cytokines (TNF-α, IL-1β, IL-6). Western blotting assessed the expression of tight junction proteins, inflammatory cytokines (TNF-α, IL-1β), and key proteins in the NF-κB pathway (IKK-α, IκB-α, NF-κB p65) in colon tissue. Results: Rats in the high-dose decoction group had slower weight gain than the control but more than other groups, with improved physical appearance and activity levels, and food and water intake similar to the control. Diarrhea rates were 50%, 17%, and 42% in the low-dose decoction, high-dose decoction, and positive control groups, respectively. Hematoxylin-eosin staining revealed intact colonic structure in the control group with orderly mucosal epithelia and no abnormalities. In the high-dose decoction group showed intact colon mucosa with minimal inflammation and no congestion or edema. DAO levels were not significantly different among groups, but D-lactate levels were significantly higher in the model group (P < 0.01), and decreased after intervention, most notably in the high-dose decoction group. After drug intervention, the colonic tight junction proteins increased, most notably in the high-dose decoction group (P < 0.01 vs. model). Serum TNF-α, IL-1β, and IL-6 levels declined, with the high-dose decoction group showing the greatest reduction (P < 0.01). And the colon’s TNF-α and IL-1β proteins followed the same trend (P < 0.01). Western blotting showed reduced expression of phosphorylated NF-κB pathway proteins (p-IKK-α, p-IκB-α, p-p65) after intervention, with the high-dose decoction group showing the greatest decrease (P < 0.01). Conclusions: Animal experiments confirm Shengyang Qushi Decoction's efficacy in treating surufatinib-induced diarrhea. It mitigates colonic tight junction damage, reduces mucosal permeability, inhibits NF-κB signaling pathway activation, and alleviates colonic inflammation. Citation Format: Huangying Tan, Shaobo Hu. Efficacy and mechanistic insights of Shengyang Qushi Decoction in managing surufatinib-associated diarrhea [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1043.

Helicobacter pylori CagA and Cag type IV secretion system activity have key roles in triggering gastric transcriptional and proteomic alterations.

Colonization of the human stomach with cag pathogenicity island (PAI)-positive Helicobacter pylori strains is associated with increased gastric cancer risk compared to colonization with cag PAI-negative strains. To evaluate the contributions of the Cag type IV secretion system (T4SS) and CagA (a secreted bacterial oncoprotein) to gastric molecular alterations relevant for carcinogenesis, we infected Mongolian gerbils with a Cag T4SS-positive wild-type (WT) H. pylori strain, one of two Cag T4SS mutant strains (∆cagT or ∆cagY), or a ∆cagA mutant for 12 weeks. Histologic staining revealed a biphasic distribution of gastric inflammation severity in WT-infected animals and minimal inflammation in animals infected with mutant strains. Atrophic gastritis (a premalignant condition), dysplasia, and gastric adenocarcinoma were only detected in WT-infected animals with high inflammation scores. Transcriptional profiling, liquid chromatography-tandem mass spectrometry analysis of micro-extracted tryptic peptides, and imaging mass spectrometry revealed more than a thousand molecular alterations in gastric tissues from WT-infected animals with high inflammation scores compared to uninfected tissues and few alterations in tissues from other groups of infected animals. Proteins with altered abundance in animals with severe Cag T4SS-induced inflammation mapped to multiple pathways, including the complement/coagulation cascade and proteasome pathway. Proteins exhibiting markedly increased abundance in tissues from H. pylori-infected animals with severe inflammation included calprotectin components, proteins involved in proteasome activation, polymeric immunoglobulin receptor (PIGR), interferon-inducible guanylate-binding protein (GBP2), lactoferrin, lysozyme, superoxide dismutase, and eosinophil peroxidase. These results demonstrate key roles for CagA and Cag T4SS activity in promoting gastric mucosal inflammation, transcriptional alterations, and proteomic alterations relevant to gastric carcinogenesis.IMPORTANCEHelicobacter pylori colonizes the stomachs of about half of humans worldwide, and its presence is the primary risk factor for the development of stomach cancer. H. pylori strains isolated from humans can be broadly classified into two groups based on whether they contain a chromosomal cag pathogenicity island, which encodes a secreted effector protein (CagA) and components of a type IV secretion system (T4SS). In experiments using a Mongolian gerbil model, we found that severe gastric inflammation and gastric transcriptional and proteomic alterations related to gastric cancer development were detected only in animals infected with a wild-type H. pylori strain containing CagA and an intact Cag T4SS. Mutant strains lacking CagA or Cag T4SS activity successfully colonized the stomach without inducing detectable pathologic host responses. These findings illustrate two different patterns of H. pylori-host interaction.

Comparative evaluation of chitligsan nanosuspension gel and spray for enhancing full-thickness wound healing in a rat model

Introduction This study explores the wound healing potential of Chitligsan (CHG), a novel formulation derived from the enzymatic and fossil-based components of Sahara soil, in nanosuspension-based gel and spray forms. Using a full-thickness wound model in Wistar rats, CHG’s efficacy was compared with saline (control) and terramycin treatments. Methods A total of 48 rats were divided into four groups: Control (saline), Spray (CHG spray), Gel (CHG gel), and Terramycin pomad. Wound areas were measured at days 3, 7, 14, and 21. Results By day 21, CHG spray reduced wound size to 0.08 ± 0.01 cm2, while the gel achieved 0.09 ± 0.01 cm2, outperforming both control (0.34 ± 0.02 cm2) and terramycin (0.14 ± 0.05 cm2, p < 0.05). Histopathological analysis demonstrated superior epithelial regeneration, dense collagenization, and minimal inflammation in CHG-treated groups compared to others. The nanoscale size of CHG particles (89.6 ± 0.26 nm) and their stable zeta potential (−26.1 ± 1.5 mV) contributed to enhanced bioavailability and wound healing efficiency. Morphological and FTIR analyses confirmed the stability and compatibility of the nanosuspension. Conclusions This study highlights CHG’s potential as a biocompatible and effective wound care solution, offering significant advantages in granulation tissue formation and keratinization compared to conventional treatments.

Discovery of Airway-Administered Ionophores for Mn2+ to Mitigate Lung Metastasis by Targeting Disseminated Tumor Cell.

Activation of the STING pathway is essential for restoring immune surveillance against dormant disseminated tumor cells (DTCs) in the lungs. Inhaled Mn2+ has potential as a STING agonist; however, its clinical application is limited by the risk of chronic inflammation and metastasis, primarily due to reactive oxygen species (ROS) generation during inhalation. To address these risks, salvianolic acid B (salB) was identified as an effective ionophore for Mn2+, enhancing STING activation while mitigating ROS-induced inflammation. In this study, salB mitigated Mn2+-induced ROS levels and enhanced STING signaling, providing a safer, noninflammatory approach to activating immune surveillance in lung DTCs. The salB-Mn2+ complexes were encapsulated in human serum albumin nanoparticles (HSA NPs) for inhalation. PET and MRI analyses revealed that intratracheal administration of HSA NP@salB-Mn2+ restricted Mn2+'s systemic distribution, retaining it primarily in the lungs and minimizing central nervous system accumulation. Subsequent lung immunofluorescence further confirmed that HSA NP@salB-Mn2+ effectively targeted lung metastatic lesions. Despite this extended retention in lung tissue, histological analysis showed minimal inflammation in mice treated with HSA NP@salB-Mn2+, in contrast to those receiving MnCl2 or MnO. Consequently, HSA NP@salB-Mn2+ demonstrated superior suppression of 4T1 cell lung metastasis in postsurgical mice relative to MnCl2 or MnO. Mechanistically, salB functions as an agonist, independently activating p-STING, which synergizes with Mn2+-induced STING activation to significantly amplify signaling and downstream target engagement. In a postsurgical mouse model, the combination of HSA NP@salB-Mn2+ and αPD-1 antibody significantly reduced DTC dormancy and enhanced immune detection, confirming its immunotherapeutic potential. These findings establish salB as a promising inhalable ionophore for Mn2+ in DTC treatment, providing three key advantages: prolonged lung retention, reduced inflammation risk, and enhanced STING-activating efficacy.

Magnetic Compression Anastomosis for Anorectal Malformations: Feasibility and Efficacy in Swine Model and Clinical Observation.

Magnetic Compression Anastomosis for Anorectal Malformations: Feasibility and Efficacy in Swine Model and Clinical Observation.

Creation of 6-10mm Diameter Transjugular Intrahepatic Portosystemic Shunts Using a Novel TIPS Stent Graft in a Swine Model

Creation of 6-10mm Diameter Transjugular Intrahepatic Portosystemic Shunts Using a Novel TIPS Stent Graft in a Swine Model

Six-Month Patency of Long Carotid Bypass Grafts Constructed with In-Body Tissue Architecture-Induced Small-Diameter Biotubes in a Goat Model.

This study investigated the long-term patency of regenerative Biotube grafts and discusses their feasibility as an alternative to autologous vein grafts for peripheral artery disease. Six Biotubes with a diameter of 4 mm were autologously fabricated in recipients using in vivo tissue engineering (in-body tissue architecture) technology and implanted as carotid artery bypass grafts in a goat model. All six grafts remained patent at 6 months despite exceeding 10 cm in length, demonstrating their biocompatibility and durability. Histological analysis revealed neointima formation, endothelialization, and minimal inflammation. However, in one goat, a graft developed stenosis, while another showed dilatation. These findings demonstrate the use of Biotubes as a viable option for peripheral vascular reconstruction as tissue-engineered vascular grafts. However, further optimization is needed to address emerging issues with their use, such as stenosis and aneurysm formation, to improve long-term patency.