Stage analysis of pancreatic ductal adenocarcinoma via network analysis.

Aim: This study aimed to introduce a biomarker panel to detect pancreatic ductal adenocarcinoma (PDAC) in the early stage, and also differentiate of stages from each other. Background: PDAC is a lethal cancer with poor prognosis and overall survival. Methods: Gene expression profiles of PDAC patients were extracted from the Gene Expression Omnibus (GEO) database. The genes that were significantly differentially expressed (DEGs) for Stages I, II, and III in comparison to the healthy controls were identified. The determined DEGs were assessed via protein-protein interaction (PPI) network analysis, and the hub-bottleneck nodes of analyzed networks were introduced. Results: A number of 140, 874, and 1519 significant DEGs were evaluated via PPI network analysis. A biomarker panel including ALB, CTNNB1, COL1A1, POSTN, LUM, and ANXA2 is presented as a biomarker panel to detect PDAC in the early stage. Two biomarker panels are suggested to recognize other stages of illness. Conclusion: It can be concluded that ALB, CTNNB1, COL1A1, POSTN, LUM, and ANXA2 and also FN1, HSP90AA1, LOX, ANXA5, SERPINE1, and WWP2 beside GAPDH, AKT1, EGF, CASP3 are suitable sets of gene to separate stages of PDAC.

Artificial intelligence and bioinformatics: a journey from traditional techniques to smart approaches.

The incorporation of AI models into bioinformatics has brought about a revolutionary era in the analysis and interpretation of biological data. This mini-review offers a succinct overview of the indispensable role AI plays in the convergence of computational techniques and biological research. The search strategy followed PRISMA guidelines, encompassing databases such as PubMed, Embase, and Google Scholar to include studies published between 2018 and 2024, utilizing specific keywords. We explored the diverse applications of AI methodologies, including machine learning (ML), deep learning (DL), and natural language processing (NLP), across various domains of bioinformatics. These domains encompass genome sequencing, protein structure prediction, drug discovery, systems biology, personalized medicine, imaging, signal processing, and text mining. AI algorithms have exhibited remarkable efficacy in tackling intricate biological challenges, spanning from genome sequencing to protein structure prediction, and from drug discovery to personalized medicine. In conclusion, this study scrutinizes the evolving landscape of AI-driven tools and algorithms, emphasizing their pivotal role in expediting research, facilitating data interpretation, and catalyzing innovations in biomedical sciences.

Evaluation of Laser Intensity Effect on Photodynamic Therapy Efficacy.

Introduction: Intensity is one of the important parameters of laser radiation in photodynamic therapy. Effective treatment requires the selection of a suitable power of laser. This study aimed to evaluate laser effectiveness in photodynamic therapy via high and low intensity by the analysis of the gene expression profiles of the treated cells. Methods: The gene expression profiles of human SK-ChA-1 cells which are treated by 500mW and 50mW laser radiation were retrieved from the Gene Expression Omnibus (GEO) database. Data were assessed by the GEO2R program, and the significant differentially expressed genes (DEGs) were investigated via expression examination and protein-protein interaction (PPI) network analysis. Results: Analyses revealed that the higher intensity of radiation is associated with wide gene expression changes relative to the lower mode. 196 significant DEGs were identified and assessed. The extremely dysregulated DEGs except MMP1 were down-regulated. STAT1, IRF7, IL1B, DDX58, ISG15, RSAD2, DHX58, OASL, OAS1, STAT2, DDX60, OAS2, USP18, and IFI44L were introduced as hubs of the main component of the PPI network. Final analysis showed that STAT1, IRF7, IL1B, DDX58, and STAT2 are the critical DEGs. Conclusion: Compared to the 50 mW mode of radiation, 500 mW laser intensity effectively changed apoptosis, differentiation, cell proliferation and angiogenesis, regulation of other inflammation-related molecules, innate immunity, and maintaining immune homeostasis.

The Effect of Photobiomodulation and Akkermansia muciniphila on THP-1 Derived Macrophage Polarization Treated with Gliadin Peptide.

Introduction: Photobiomodulation (PBM) and Akkermansia muciniphila have been shown to be effective in improving inflammatory conditions with positive effects on increasing the population of anti-inflammatory M2 macrophages (MQs). In this study, gliadin-stimulated THP-1 derived MQs were treated with A. muciniphila and PBM to evaluate their effects on promoting the polarization of M2 MQs. Methods: The human monocyte cell line (THP-1) was differentiated to MQs. MQs were stimulated with 200 µg/mL gliadin for 24 hours and then treated with PBM 810 nm alone and in combination with A. muciniphila for the following 24 hours to evaluate their effects on MQs polarization. THP-1 derived MQs were also treated with PBM and A. muciniphila to evaluate their effects on non-stimulated MQs. CD11b, CD80, and CD206 levels were evaluated by using the flow cytometry technique. Moreover, the expression of some M1 and M2-related cytokines was determined. Results: PBM therapy of gliadin-stimulated MQs decreased IL-6 and increased TGF-ß, IL-10 and TNF-α expression compared with gliadin exposed MQs. PBM along with A. muciniphila treatment induced IL-6, TNF-α, and IL-10 expression in MQs in comparison to the untreated group. It also elevated TGF-ß, IL-10 and TNF-α levels in gliadin-triggered MQs in comparison to gliadin-stimulated MQ cells. Conclusion: The result of this study showed the potential of PBMT and A. muciniphila for modulating inflammatory responses and MQs polarization. This may open new perspectives to find possible therapeutic targets for celiac diseases.

Assessment of NB-UVB Effects on Skin of Atopic Dermatitis Patients: A Network Analysis.

Introduction: Atopic dermatitis is a common inflammatory skin disease which is treated with narrowband ultraviolet B (NB-UVB). Exploring the critical targeted genes in patients by UV radiation is the main aim of this study. Methods: Gene expression profiles of lesional and non-lesional skin samples of atopic dermatitis patients after treatment with NB-UVB and the non-irradiated samples were extracted from the Gene Expression Omnibus (GEO) database and analyzed via protein-protein interaction (PPI) network analysis to find the critical targeted genes. Results: A total of 357 significant differentially expressed genes (DEGs) were included in the PPI network. CTNNB1, SRSF1, YWHAB, SMC3, GNB2, ARF3, UBL7, RAB2A, YWHAE, EIF5B, SNRPE, PPIG, RC3H2, CFL1, SMARCB1. LAPTM5, PRPF40A, and RBBP4 were introduced as hub-bottlenecks. Conclusion: In conclusion, five central genes including SMC3, ARF3, EIF5B, SMARCB1, and LAPTM5 were highlighted as the critical genes in response to NB-UVB radiation in the skin of the treated atopic dermatitis patients. The introduced crucial genes are involved in essential cellular functions such as apoptosis, cell cycle, cell proliferation, and inflammation. It seems that applied NB-UVB radiation is a suitable therapeutic method for atopic dermatitis disease.

Efficacy Evaluation of Treatment of Psoriasis Via Narrow Band-Ultraviolet Radiation.

Introduction: Psoriasis is a common autoimmune skin disease associated with genetically influenced chronic inflammation accompanied by remitting and deteriorating scaly skin. T-cell targeted biologics, IL-17 inhibitors, IL-12/IL-23 inhibitors, TNF-α inhibitors, PDE4 inhibitors, and ultraviolet (UV) radiation are applied to treat psoriasis. Efficacy evaluation of narrow band UVB (NB-UVB) radiation was the aim of this study. Methods: Data were extracted from Gene Expression Omnibus (GEO) and were pre-evaluated via the GEO2R program. The significant differentially expressed genes (DEGs) were included in the protein-protein interaction (PPI) network analysis. The hubs, bottlenecks, and hub-bottleneck DEGs were introduced as central genes. Activation, inhibition, and expression relationship between central genes were assessed to explore the critical individuals. Results: Among 513 analyzed significant DEGs, 22 hub-bottleneck genes were identified. Further analysis revealed that FN1, STAT3, HIF1A, IL1B, P4HB, SOD2, MMP2, and STAT1 were the crucial genes in psoriasis samples targeted by NB-UVB radiation. Conclusion: In conclusion, NB-UVB radiation as a treatment targets critical genes in peri-lesion skin tissue biopsy of psoriasis patients via a complicated mechanism. This therapeutic method downregulates STAT3, HIF1A, IL1B, and P4HB to treat psoriasis but downregulates STAT1 and SOD2 and upregulates MMP2 and FN1 to develop disease.

The role of tryptophan metabolism and tolerogenic dendritic cells in maintaining immune tolerance: Insights into celiac disease pathogenesis.

BACKGROUND: In mammals, amino acid metabolism has evolved to control immune responses. Tryptophan (Trp) is the rarest essential amino acid found in food and its metabolism has evolved to be a primary regulatory node in the control of immune responses. Celiac disease (CeD) is a developed immunological condition caused by gluten intolerance and is linked to chronic small intestine enteropathy in genetically predisposed individuals. Dendritic cells (DCs), serving as the bridge between innate and adaptive immunities, can influence immunological responses in CeD through phenotypic alterations. OBJECTIVE: This review aims to highlight the connection between Trp metabolism and tolerogenic DCs, and the significance of this interaction in the pathogenesis of CeD. RESULTS: It is been recognized that various DC subtypes contribute to the pathogenesis of CeD. Tolerogenic DCs, in particular, are instrumental in inducing immune tolerance, leading to T-reg differentiation that helps maintain intestinal immune tolerance against inflammatory responses in CeD patients and those with other autoimmune disorders. T-regs, a subset of T-cells, play a crucial role in maintaining intestinal immunological homeostasis by regulating the activities of other immune cells. Notably, Trp metabolism, essential for T-reg function, facilitates T-reg differentiation through microbiota-mediated degradation and the kynurenine pathway. CONCLUSION: Therefore, alterations in Trp metabolism could potentially influence the immune response in CeD, affecting both the development of the disease and the persistence of symptoms despite adherence to a gluten-free diet.

Extracellular vesicles and cancer stem cells: a deadly duo in tumor progression.

The global incidence of cancer is increasing, with estimates suggesting that there will be 26 million new cases and 17 million deaths per year by 2030. Cancer stem cells (CSCs) and extracellular vesicles (EVs) are key to the resistance and advancement of cancer. They play a crucial role in tumor dynamics and resistance to therapy. CSCs, initially discovered in acute myeloid leukemia, are well-known for their involvement in tumor initiation, progression, and relapse, mostly because of their distinct characteristics, such as resistance to drugs and the ability to self-renew. EVs, which include exosomes, microvesicles, and apoptotic bodies, play a vital role in facilitating communication between cells within the tumor microenvironment (TME). They have a significant impact on cellular behaviors and contribute to genetic and epigenetic changes. This paper analyzes the mutually beneficial association between CSCs and EVs, emphasizing their role in promoting tumor spread and developing resistance mechanisms. This review aims to investigate the interaction between these entities in order to discover new approaches for attacking the complex machinery of cancer cells. It highlights the significance of CSCs and EVs as crucial targets in the advancement of novel cancer treatments, which helps stimulate additional research, promote progress in ideas for cancer treatment, and provide renewed optimism in the effort to reduce the burden of cancer.

Assessment of Recovery Time Effects on Human Primary Neonatal Dermal Fibroblasts After Exposure to Solar-Simulated Ultraviolet Radiation.

Introduction: Photoaging that is accompanied by gene expression alteration is known as early aging of the skin due to overexposure to natural and/or artificial ultraviolet radiation (UVR). The assessment of gene expression alteration in human primary neonatal dermal fibroblasts depending on recovery time after exposure to solar simulated ultraviolet radiation (ssUVR) is the main aim of this bioinformatic study. Methods: Data are extracted from Gene Expression Omnibus (GEO). The pre-evaluation is done via the GEO2R program. The Significant differentially expressed genes (DEGs) were assessed via protein-protein interaction (PPI) network analysis, and the central genes were identified. The central genes were enriched via gene ontology assessment. Results: Among 224 significant DEGs, 20 central genes including TOP2A, MKI67, BRCA1, HELLS, MAD2L1, ANLN, KIF11, MSH2, KRAS, NCAPG, RFC3, PLK4, WDHD1, BLM, CDKN3, KIF15, SMARCA5, and ATAD2 as hub genes and TOP2A, MKI67, BRCA1, ANLN, KRAS, PLK4, SMARCA5, MMP2, and TLR4 as bottleneck genes were determined. Eight central genes were associated with 16 biological terms. Conclusion: In conclusion, significant differences appeared between gene expression conditions of the cells after 1-day and 5-day recovery. Molecular events include the repair and continuation of photodamages. It is possible to introduce drug targets to prevent the progress of induced damages.

Evaluation of Near-Infrared Laser Effects on 143B Cells: A System Biology Approach.

Introduction: Photothermal therapy (PTT) by using a near-infrared (NIR) laser, as a successful treatment of cancer, has attracted extensive attention of researchers. Its advantages as a noninvasive and suitable method have been confirmed. Discovery of the NIR laser molecular mechanism at the cellular level via system biology assessment to identify the crucial targeted genes is the aim of this study. Methods: RNA-seq series of six samples were retrieved from Gene Expression Omnibus (GEO) and pre-evaluated by the GEO2R program for more analysis. The significant differentially expressed genes (DEGs) were determined and studied via gene expression analysis, protein-protein interaction (PPI) network assessment, action map evaluation, and gene ontology enrichment. Results: HSPA5, DDIT3, TRIB3, PTGS2, HMOX1, ASNS, GDF15, SLC7A11, and SQSTM1 were identified as central genes. Comparing the central genes and the determined crucial genes via gene expression analysis, actin map results, and gene ontology enrichment led to the introduction of HSPA5, DDIT3, PTGS2, HMOX1, and GDF15 as critical genes in response to the NIR laser. Conclusion: The results indicated that the principle biological process "Endoplasmic reticulum unfolded protein response" and HSPA5, DDIT3, PTGS2, HMOX1, and GDF15 are the crucial targets of the NIR laser. The results also showed that the NIR laser induces stress conditions in the irradiated cells.

Evaluation of genetic association between celiac disease and type 1 diabetes.

Purpose: Celiac disease (CD) is a chronic autoimmune disorder with a common genetic pathogenesis with type 1 diabetes (T1D). This study aimed to investigate the immune regulation in patients with both CD and T1D. Methods: A total of 29 CD patients, 29 T1D patients, and 16 patients with both CD and T1D, along with 30 healthy controls (HCs) were included. The mRNA expression levels of TNF-α, IL-6, IL-2, and CTLA4 were evaluated in peripheral blood samples. Results: The results showed that in patients with CD, T1D and CD/T1D, TNF-α mRNA levels were significantly increased (P = 0.0009, 0.0001, and 0.008, respectively), while CTLA4 mRNA levels were significantly decreased in them compared to the control group (P = 0.0009, 0.0001, and 0.004, respectively). IL-2 mRNA expression levels were also significantly higher in CD (P = 0.01) and comorbid CD/T1D (P = 0.01) patients than in the control group. There was no significant difference in terms of IL-6 expression between studied groups (P > 0.05). Conclusions: TNF-α mRNA exhibited potential diagnostic value for distinguishing CD, T1D, and comorbid CD/T1D patients from HCs. These findings contribute to our understanding of the shared genetic factors and potential mechanisms underlying CD and T1D, which can aid in improved diagnostic methods and treatment approaches for these conditions.

Inflammation and immunological disarrays are associated with acute exercise in type 2 diabetes.

Objective: Type 2 diabetes (T2D) is the most common metabolic disorder that is associated with insulin resistance. The aim of the present study is to discover details of the molecular mechanism of exercise on control or progress of diabetic condition in patients via network analysis. Methods: Gene expression profiles of patients with T2D before and after doing exercise are retrieved from Gene Expression Omnibus (GEO) and are pre-evaluated by the GEO2R program. Data are studied based on expression values, regulatory relationships between the differentially expressed genes (DEGs), gene ontology analyses, and protein-protein interaction PPI network analysis. Results: A number of 118 significant DEGs were identified and classified based on fold change (FC) values as most dysregulated genes and dysregulated individuals. Action map analysis revealed that 18 DEGs appeared as the critical genes. Gene ontology analysis showed that 24 DEGs are connected to at least four pathways. JUN, IL6, IL1B, PTGS2, FOS, MYC, ATF3, CXCL8, EGR1, EGR2, NR4A1, PLK3, TTN, and UCP3 were identified as central DEGs. Conclusion: Finally; JUN, IL6, IL1B, PTGS2, FOS, ATF3, CXCL8, EGR1, and EGR2 were introduced as the critical targeted genes by exercise. Since the critical genes after exercise are upregulated and mostly are known as the risk factors of T2D, it can be concluded that unsuitable exercise can develop diabetic conditions in patients. Acute exercise-induced inflammation and immune disturbances seem to be associated with the development of T2D in patients.

Diagnostic and Prognostic Value of miR-451 Expression in Colorectal Cancer: A Meta-Analysis.

BACKGROUND: The miR-451 has been reported to play an important role in colorectal cancer (CRC) pathogenesis and can be a pivotal diagnosis biomarker of CRC. Given the contradictions in the diagnosis value of the miR-451 in patients with CRC, deciphering the diagnostic/prognostic role of this miRNA in CRC will support the identification of a novel therapeutic target for CRC. Therefore, in the present meta-analysis, we evaluated the diagnostic value of miR-451 in CRC patients. MATERIALS AND METHODS: The electronic databases of Embase, PubMed, ISI Web of Science, and Scopus systematically searched for relevant studies. The odds ratio (OR) with a 95% confidence interval (CI) was calculated to evaluate the association between miR-451 family expression and diagnosis of colorectal cancer. The parameters including sensitivity, specificity, and area under the curve (AUC) were obtained. The quality of evidence was evaluated using the Newcastle-Ottava Scale (NOS). RESULTS: This study involved 510 patients (45% female and 55% male) with CRC. The pooled analysis of the studies showed a significant association between low expression levels of miR-451 in patients with CRC (OR = 7.59; 95% CI 2.39 - 24.07; p = 0.001). The overall sensitivity and specificity were 0.95 (0.61 - 1) and 0.83 (0.43 - 0.99), respectively. The pooled AUC was 0.97 (0.88 - 1; p < 0.006). Results showed if the pre-test probability is 50% for a patient, the post-test probability will be 85%. The indices demonstrated the high potency of miR-451 as a diagnostic biomarker in patients with CRC. No publication bias was observed using the Begg's (p=0.85) and Egger's tests (p=0.45). CONCLUSION: A strong relationship between the low expression levels of miR-451 and CRC progression was observed. This finding suggests the miR-451 family may be helpful as a potential biomarker for the earlier diagnosis of colorectal cancer.

The Potential Role of Intestinal Stem Cells and Microbiota for the Treatment of Colorectal Cancer.

Colorectal cancer is a global health concern with high incidence and mortality rates. Conventional treatments like surgery, chemotherapy, and radiation therapy have limitations in improving patient survival rates. Recent research highlights the role of gut microbiota and intestinal stem cells in maintaining intestinal health and their potential therapeutic applications in colorectal cancer treatment. The interaction between gut microbiota and stem cells influences epithelial self-renewal and overall intestinal homeostasis. Novel therapeutic approaches, including immunotherapy, targeted therapy, regenerative medicine using stem cells, and modulation of gut microbiota, are being explored to improve treatment outcomes. Accordingly, this chapter provides an overview of the potential therapeutic applications of gut microbiota and intestinal stem cells in treating colorectal cancer.

Introducing critical proteins related to liver ischemia/reperfusion injury.

Aim: The current study aimed to introduce the key proteins involved in liver ischemia/reperfusion (I/R) injury through protein-protein interaction (PPI) analysis. Background: Liver transplantation (LT) is a well-known treatment for liver diseases that threaten patients with mortality. LT is a complex operation, and several risks, including liver I/R injury, affect its success. Improving LT requires detection of its molecular mechanism. Experiments have revealed that high throughput methods such as proteomics in combination with bioinformatics are useful tools for analyzing the molecular mechanism of disease. Methods: The differentially expressed proteins (DEPs) involved in liver I/R injury were extracted from the literature. The queried DEPs plus the first 100 neighbors were included in a network through STRING database using Cytoscape software. Degree, betweenness centrality, closeness centrality, and stress were considered to determine the central nodes. The queried DEPs were assessed by action map analysis using the CluePedia application of Cytoscape software. The key proteins were identified by comparing network analysis and action map evaluation results. Results: Six proteins, namely ALB, INS, GAPDH, CAT, IL6, and TNF, among the added first neighbors were determined as the central first neighbors. MPO, CRP, MMP9, and HMOX1 were selected as central DEPs among the queried proteins. Action map analysis confirmed the PPI findings. The final evaluation revealed that MMP9 in combination with CRP and HMOX1 plays a critical role in liver I/R injury. Conclusion: The significant role of MMP9 in liver I/R injury was detected in this study. Two central proteins (CRP and HMOX1) were shown to have a regulatory effect on MMP9; CRP activated MMP9, while HMXO1 downregulated it.

The connection between fatty acids and inflammation in celiac disease; a deep exploring.

The interplay between fatty acids (FAs) and celiac disease (CD) is a burgeoning field of research with significant implications for understanding the pathophysiology and potential therapeutic avenues for this autoimmune disorder. CD, triggered by gluten consumption in susceptible individuals, presents with a range of intestinal and extra-intestinal symptoms impacting various bodily functions. The disruption of intestinal tight junctions (TJs) by gluten proteins leads to increased gut permeability and subsequent inflammatory responses mediated by T-cells. FAs, crucial components of cell membranes, play diverse roles in inflammation and immune regulation. In fact, FAs have been shown to modulate inflammatory processes through various mechanisms. Studies have highlighted alterations in FA profiles in individuals with CD, indicating potential implications for disease pathogenesis and micronutrient deficiencies. Moreover, the exploration of FAs as biomarkers for CD diagnosis offers promising avenues for future research and therapeutic interventions. Understanding the intricate relationship between FAs and CD could lead to novel approaches in managing this complex autoimmune disorder. Therefore, this review article aims to provide an overview of the connection between FAs and inflammation in CD.

Isolation and Phenotypic Characterization of Tumor-Infiltrating NK Cells in Skin Carcinoma.

In oncological research, the function of tumor-infiltrating natural killer (NK) cells in skin carcinoma presents a viable avenue for novel therapeutic methods. NK cells are essential to the body's defense against malignancies, including skin cancer, and are especially important in more sophisticated cancer immunotherapies such as vaccinations containing dendritic cells. The deadliest type of skin cancer, malignant melanoma, still has a poor prognosis even with advancements in early-stage therapies, which emphasizes the need for novel therapeutic strategies. NK cells from human melanoma metastases were subjected to single-cell RNA-seq analysis, which demonstrated notable variations in the transcriptional programs of tumor-infiltrating and circulating NK cells. Different transcriptional states are displayed by NK cells that have invaded tumors, indicating that they are functionally specialized in areas like chemokine production and cytotoxicity. These results emphasize the functions of NK cells in recruiting other significant immune cell types, such as cross-presenting dendritic cells, and in direct cytotoxicity against malignant cells. Investigating NK cells that infiltrate tumors in skin carcinomas presents a viable approach to comprehending and may be modifying the immune environment surrounding these cancers. It is essential to comprehend the distinct characteristics and roles of NK cells inside the tumor microenvironment in order to create more potent immunotherapeutic approaches to treat skin cancer. In order to perhaps open the door for new directions in cancer immunotherapy, the project intends to establish a thorough technique for the isolation and thorough phenotypic characterization of tumor-infiltrating NK cells in skin carcinoma.

Standardized GMP-Compliant Scalable 3D-Bioprocessing of Epidermal Stem Cells for Diabetic Foot Ulcers.

Diabetic foot ulcers (DFUs) pose a significant threat to the health and well-being of individuals with diabetes, often leading to lower limb amputations. Fortunately, epidermal stem cell therapy offers hope for improving the treatment of DFUs. By leveraging 3D culture techniques, the scalability of stem cell manufacturing can be greatly enhanced. In particular, using bioactive materials and scaffolds can promote the healing potential of cells, enhance their proliferation, and facilitate their survival. Furthermore, 3D tissue-mimicking cultures can accurately replicate the complex interactions between cells and extracellular matrix, thereby ensuring that the stem cells are primed for therapeutic application. To ensure the safety and quality of these stem cells, it is essential to adhere to good manufacturing practice (GMP) principles during cultivation. This chapter provides a comprehensive overview of the step-by-step process for GMP-based 3D epidermal stem cell cultivation, thus laying the groundwork for developing reliable regenerative medicine therapies.

Acellular Fish Skin for Deep Dermal Traumatic Wounds Management; Introducing a Novel Dressing.

The optimal therapy for deep wounds is based on the early debridement of necrotic tissue followed by wound coverage to avoid a systemic inflammatory response and optimize scar-free healing. The outcomes are affected by available resources and underlying patient factors, which cause challenges in wound care and suboptimal outcomes. Here we report a patient with deep dermal injury wounds, who was treated with platelet-rich fibrin (PRF) gel, plasma rich in growth factor (PRGF) gel, and acellular fish skin. Patient's outcomes regarding healing and scar quality were collected objectively and subjectively for one year after the injury. Wounds treated with acellular fish skin demonstrated accelerated wound healing, a significantly higher water-storage capacity, and better pain relief. Furthermore, improved functional and cosmetic outcomes, such as elasticity, skin thickness, and pigmentation, were demonstrated. It seems that, the PRGF gel and PRF in combination with acellular fish skin grafts resulted in the faster healing of wounds and better functional and aesthetic outcomes than split-thickness skin grafts treatment.

Intestinal mRNA expression analysis of polarity-related genes identified the discriminatory ability of CRB3 as a diagnostic marker for celiac disease.

BACKGROUND: Celiac disease (CD) is a chronic autoimmune disorder characterized by an abnormal immune response to gluten, a protein found in wheat, barley, and rye. It is well established that the integrity of epithelial tight junctions (TJs) and adherens junctions (AJs) plays a crucial role in the pathogenesis of CD. These junctional complexes contribute to the apical-basal polarity of the intestinal epithelial cells, which is crucial for their proper functioning. METHODS: Sixty CD subjects, and 50 controls were enrolled in the current study. Mucosal samples were obtained from the distal duodenum, total RNA was extracted and complementary DNA was synthesized. The relative expression levels of the desired genes were evaluated by quantitative real-time polymerase chain reaction based on ΔΔCt method. The gene-gene interaction network was also constructed using GeneMANIA. RESULTS: CRB3 (p = .0005), LKB1 (p < .0001), and SCRIB (p = .0005) had lower expression in CD patients compared to controls, while PRKCZ expression did not differ between groups (p > .05). CRB3 represented a significant diagnostic value for differentiating CD patients from the control group (p = .02). CONCLUSION: The aim of the current study was to evaluate the changes in the mRNA expression levels of SCRIB, PRKCZ, LKB1, and CRB3 genes in the small intestinal biopsy samples of CD patients in comparison to the healthy control subjects. Our data uncover the importance of polarity-related genes (especially CRB3) in CD pahtomechanism, that may facilitate the planning of the future studies looking for finding innovative diagnostic and therapeutic strategies for CD.