Interstitial Cells Of Cajal Research Articles

Gastrointestinal stromal tumors: a focus on the impact of interstitial cells of Cajal in disease development

Gastrointestinal stromal tumors: a focus on the impact of interstitial cells of Cajal in disease development

Conditional deletion of IP3R1 by Islet1-Cre in mice reveals a critical role of IP3R1 in interstitial cells of Cajal in regulating GI motility.

Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) has been proposed to play a physiological role in regulating gastrointestinal (GI) motility, but the underlying cell-dependent mechanism remains unclear. Here, we utilized cell-specific IP3R1 deletion strategies to address this question in mice. Conditional IP3R1 knockout mice using Wnt1-Cre, Islet1-Cre mice, and smMHC-CreEGFP were generated. Cell lineage tracing was performed to determine where gene deletion occurred in the GI tract. Whole-gut transit assay and isometric tension recording were used to assess GI function in vivo and in vitro. In the mouse GI tract, Islet1-Cre targeted smooth muscle cells (SMCs) and interstitial cells of Cajal (ICCs), but not enteric neurons. IP3R1 deletion by Islet1-Cre (isR1KO) caused a phenotype of intestinal pseudo-obstruction (IPO), evidenced by prolonged whole-gut transit time, enlarged GI tract, abdominal distention, and early lethality. IP3R1 deletion by Islet1-Cre not only reduced the frequency of spontaneous contractions but also decreased the contractile responses to the muscarinic agonist carbachol (CCh) and electrical field stimulation (EFS) in colonic circular muscles. By contrast, smMHC-CreEGFP only targeted SMCs in the mouse GI tract. Although IP3R1 deletion by smMHC-CreEGFP (smR1KO)also reduced the contractile responses to CCh and EFS in colonic circular muscles, the frequency of spontaneous contractions was less affected, and neither global GI abnormalities nor early lethality was found in smR1KO mice. IP3R1 deletion in both ICCs and SMCs but not in SMCs alone causes an IPO phenotype, suggesting that IP3R1 in ICCs plays an essential role in regulating GI motility in vivo.

Structural Alterations in Diverticular Disease

AbstractClinicians appreciate the structural alterations of diverticular disease when navigating narrow, angulated colons with a colonoscope or removing stiff, fixed sigmoid colons at surgery. Investigation of these tissues reveals increased thickness of smooth muscle, alterations in the amount and structure of the extracellular matrix, and changes to the motility of the colon. More sophisticated technologies now allow scientists to unravel the connections between these alterations and the individual genetic background. This article explores the structural alterations of diverticular disease including collagen, smooth muscle, the enteric nervous system, and the interstitial cells of Cajal.

Calcium wave dynamics in the embryonic mouse gut mesenchyme: impact on smooth muscle differentiation

Intestinal smooth muscle differentiation is a complex physico-biological process involving several different pathways. Here, we investigate the properties of Ca2+ waves in the developing intestinal mesenchyme using GCamp6f expressing mouse embryos and investigate their relationship with smooth muscle differentiation. We find that Ca2+ waves are absent in the pre-differentiation mesenchyme and start propagating immediately following α-SMA expression. Ca2+ waves are abrogated by CaV1.2 and gap-junction blockers, but are independent of the Rho pathway. The myosine light-chain kinase inhibitor ML-7 strongly disorganized or abolished Ca2+ waves, showing that perturbation of the contractile machinery at the myosine level also affected the upstream Ca2+ handling chain. Inhibiting Ca2+ waves and contractility with CaV1.2 blockers did not perturb circular smooth muscle differentiation at early stages. At later stages, CaV1.2 blockers abolished intestinal elongation and differentiation of the longitudinal smooth muscle, leading instead to the emergence of KIT-expressing interstitial cells of Cajal at the gut periphery. CaV1.2 blockers also drove apoptosis of already differentiated, CaV1.2-expressing smooth muscle and enteric neural cells. We provide fundamental new data on Ca2+ waves in the developing murine gut and their relation to myogenesis in this organ.

Characterization of the cellular components of mouse collecting lymphatic vessels reveals that lymphatic muscle cells are the innate pacemaker cells regulating lymphatic contractions.

Collecting lymphatic vessels (cLVs) exhibit spontaneous contractions with a pressure-dependent frequency, but the identity of the lymphatic pacemaker cell is still debated. By analogy to pacemakers in the GI and lower urinary tracts, proposed cLV pacemaker cells include interstitial cells of Cajal like cells (ICLC) or the lymphatic muscle (LMCs) cells themselves. Here we combined immunofluorescence and scRNAseq analyses with electrophysiological methods to examine the cellular constituents of the mouse cLV wall and assess whether any cell type exhibited morphological and functional processes characteristic of pacemaker cells: a continuous if not contiguous network integrated into the electrical syncytium; spontaneous Ca2+ transients; and depolarization-induced propagated contractions. We employed inducible Cre (iCre) mouse models routinely used to target these specific cell populations including: c-kitCreER T2 to target ICLC; PdgfrβCreER T2 to target pericyte-like cells; PdgfrαCreER ™ to target CD34+ adventitial cells and ICLC; and Myh11CreER T2 to target LMCs directly. These specific inducible Cre lines were crossed to the fluorescent reporter ROSA26mT/mG, the genetically encoded Ca2+ sensor GCaMP6f, and the light-activated cation channel rhodopsin2 (ChR2). c-KitCreER T2 labeled both a sparse population of LECs and round adventitial cells that responded to the mast cell activator compound 48-80. PdgfrβCreER T2 drove recombination in both adventitial cells and LMCs, limiting its power to discriminate a pericyte-specific population. PdgfrαCreER ™ labeled a large population of interconnected, oak leaf-shaped cells primarily along the adventitial surface of the vessel. Of these cells, only LMCs consistently, but heterogeneously, displayed spontaneous Ca2+ events during the diastolic period of the contraction cycle, and whose frequency was modulated in a pressure-dependent manner. Optogenetic depolarization through the expression of ChR2 under control of Myh11CreER T2 , but not PdgfrαCreER ™ or c-KitCreER T2 , resulted in propagated contractions upon photo-stimulation. Membrane potential recordings in LMCs demonstrated that the rate of diastolic depolarization significantly correlated with contraction frequency. These findings support the conclusion that LMCs, or a subset of LMCs, are responsible for mouse cLV pacemaking.

Immunohistochemical localization and distribution of Cajal cell in the intestine of rabbit

Immunohistochemical localization and distribution of Cajal cell in the intestine of rabbit

Histological and histochemical study of effect of dietary fibre in motility of stomach in male mice.

To investigate the relationship between dietary fibres and muscularis externa layer. The experimental study was conducted at the Anatomy Department of the College of Medicine, Al- Nahrain University, Iraq, from November 2020 to April 2021, and comprised adult healthy males. They were divided randomly into experimental group A and control group B. Group A was fed high-fibre diet, and group B was fed standard pellet diet. The tissue samples were harvested at day 30 post-surgery. The stomach samplings were placed in 10% neutral formalin for 24 hours to obtain paraffin sections for routine histological and immunohistochemical staining. The protein expression in stomach's smooth muscle of each group was detected by immunohistochemical staining. Data was analysed using SPSS 24. Of the 20 mice, 10(50%) were in each of the two groups. Group A exhibited significant weight-gain compared to group B (p≤0.01). There was significant reduction in the thickness of the muscularis layer in group A compared to group B (p≤0.01). Anoctamin 1 expression in group A was significantly lower than that in group B (p≤0.01). The stress induced by an unstable fibre diet significantly affected the stomach by decreasing the muscularis layer thickness and Anoctamin 1 expression in interstitial cells of Cajal.

Effects of protein diet on expression of Anoctamin1 of Cajal cell in the nervous plexus of the stomach in male mice.

To determine the association between a protein-rich diet and the expression of anoctamin 1 in Interstitial cells of Cajal within the muscle layer of the stomach wall in male mice. The experimental study was conducted at the Anatomy Department of the College of Medicine, Al- Nahrain University, Iraq, from November 2020 to April 2021, and comprised male adult healthy male mice. They were divided randomly into two equal groups. Group A was fed a high protein diet, while control group B was fed a standard pellet diet. The tissue samples were harvested at day 30 post-surgery. The stomach samplings were placed in 10% neutral formalin for 24 hours to obtain paraffin sections for routine histological and immunohistochemical staining. The protein expression in stomach smooth muscle of each group was detected by immunohistochemical staining. Data was analysed using SPSS 24. Of the 20 mice, 10(50%) were in each of the two groups. Group A exhibited significant weight-gain compared to group B (p≤ 0.05). There was significant elevation in muscle wall thickness in group A, compared to group B (p≤0.05). Tunica muscularis of the stomach in group A significantly thickened compared to group B (p≤0.05). The expression of anoctamin 1 was significantly more intense in group A compared to group B (p≤0.01). Unbalanced food had a significant impact on the stomach, affecting the thickness of the muscularis layer and the expression of anoctamin 1 in cajal cells in the muscularis externa.

Exploring the heterogeneity of interstitial cells of Cajal and their properties in gastrointestinal mesenchymal tumors applying single-cell RNA sequencing analysis

BackgroundGastrointestinal mesenchymal stromal tumors (GISTs) are a group of intramural tumors that exhibit a wide range of morphologies. Dysfunction or loss of interstitial cells of Cajal (ICCs) is correlated with the disorders of gastrointestinal motility. At present, the characterization and molecular mechanisms underlying the role of ICCs in GIST are still not clear.MethodsThe GSE162115 dataset from Gene Expression Omnibus database was processed using Seurat package for quality control, data normalization, and cell clustering. Differential expression and functional enrichment analyses were performed using the FindAllMarkers function and clusterProfiler package. Cellular heterogeneity was assessed by CytoTRACE and potential regulatory mechanisms of ICCs in GISTs were investigated using SCENIC. Cellular communication was inferred and analyzed applying the CellChat package.ResultsEight clusters were identified based on 34,861 cells. Intra-tumor samples had a higher proportion of ICCs than peri-tumor. ICCs were related to cell cycle and glycolytic activity in intra-tumor samples, while those in peri-tumor samples were involved in immune response. Further analysis identified four ICC subgroups (subcluster 1–4), of which subcluster 3 showed the most typical stem cell properties and interacted with the rest of the cells through the MIF-CD74 (CD44) protein.ConclusionThis study analyzed the heterogeneity and stem cell properties of ICCs in GISTs, revealing the molecular mechanisms and potential therapeutic targets for GISTs.

Immunohistochemical evaluation of CD34, CD117, and calretinin for diagnosis of hirschsprung’s disease

IntroductionHirschsprung’s disease (HD) is a neurogenic intestinal disorder attributed to incomplete neural crest cell migration during fetal intestinal development, leading to an aganglionic segment of the colon and functional obstruction. Associated malformations like intestinal atresia, hydronephrosis, and imperforate anus can accompany Hirschsprung’s disease. this study aims to evaluate the efficacy of Calretinin and Cajal cells (CD34 and CD117) immunohistochemical staining in improving HD diagnosis.MethodsThe study involved 70 pediatric patients suspected of Hirschsprung’s disease. Clinical, histopathological, and immunohistochemical analyses were conducted, focusing on calretinin, CD34, and CD117 markers to identify ganglion cells and Cajal cells. Data were statistically analyzed using SPSS software.ResultsIn the examination of the samples, the calretinin marker exhibited a consistent accuracy of 100% in diagnosing Hirschsprung’s disease (with sensitivity and specificity both at 100%). Regarding the markers for Cajal cells in cases of Hirschsprung’s disease, an irregularity in the arrangement of Cajal cells was observed, which was absent in normal cases. These markers also demonstrated a specificity and sensitivity of 100% in diagnosing the disease.ConclusionHirschsprung’s disease remains a complex condition with multifaceted pathophysiological mechanisms. Calretinin immunohistochemical staining offers enhanced diagnostic accuracy, while the debate surrounding ICC distribution underscores the need for advanced diagnostic techniques. Further research is warranted to unravel the intricacies of Hirschsprung’s disease and its associated complications.

Emodin repairs interstitial cells of Cajal damaged by cholelithiasis in the gallbladder.

Hypercholesterolemia induces cholelithiasis and dysfunction of gallbladder motility. Interstitial cells of Cajal (ICCs) contribute to gallbladder motility. Emodin modulates the contractility of the gallbladder muscle; however, the underlying mechanism is unknown. This study aimed to explore the effects of emodin on gallbladder ICCs with cholelithiasis in a guinea pig model. Animals were randomly divided into a healthy control group and three study groups. All study groups received a high-cholesterol diet (HCD) for 8 weeks. Subsequently, they were randomly assigned to either the HCD group or one of the emodin treatment groups lasting 4 or 8weeks. Total cholesterol (TC) and triglycerides (TG) were measured to determine changes in serum lipid levels. Immunohistochemistry was performed to detect the morphology and number of ICCs. TUNEL assays were performed to detect ICC apoptosis. Transmission electron microscopy was employed to observe ICC structure. Western blotting and real-time polymerase chain reaction were used to detect changes in stem cell factor (SCF)/c-kit pathway expression. Serum TC and TG were higher in all study groups. In cases of cholelithiasis, the SCF/c-kit pathway was downregulated, the number of gallbladder ICCs decreased, apoptosis increased, and the ICC network structure was damaged. After emodin treatment, the SCF/c-kit pathway was upregulated, the number of gallbladder ICCs increased, apoptosis decreased, and the ICC network structure recovered. Cholelithiasis downregulates the SCF/c-kit pathway and damages gallbladder ICCs. Emodin upregulates the SCF/c-kit pathway and increases gallbladder ICCs, contributing to recovery from gallbladder motility disorders.\.

Role of Interstitial Cells of Cajal in Congenital Ureteropelvic Junction Obstruction.

Although congenital ureteropelvic junction (UPJ) obstruction is the most common cause of neonatal hydronephrosis, aetiopathogenesis is still inconclusive. Recently, the paucity of interstitial cells of Cajal (ICC) at the narrow adynamic part of UPJ has been implicated as a causative factor. This prospective study was conducted between October 2019 and March 2022 to find out the density of ICC by the immunohistochemical method using CD117 (c-kit) antibody, in resected segments of UPJ in obstruction patients and in renal tumour patients as control. ICC/high power field (hpf) was also studied from the margins of the resected segment in the obstruction group. The pre-operative and post-operative sonographic and renal scintigraphic features were compared. The median age of patients in the study group (n = 25) was 36 months and in the control group was 39 months. The mean ICC/hpf at the stenotic part of UPJ in the study group was 3.56 ± 1.26 and in the control group was 12.56 ± 1.89 (P = 0.0001). ICC density from the proximal and distal margins of the resected segment was 11.12 ± 2.12 and 11.68 ± 1.62, respectively (P < 0.001). The post-operative antero-posterior diameter of the renal pelvis and differential renal function showed significant improvement in comparison to the pre-operative value (P = 0.0045 and 0.0005, respectively). The significant decrease in the density of ICC at the stenotic part of UPJ compared to controls suggests a pacemaker role of these cells in ureteral peristalsis and the aetiopathogenesis of UPJ obstruction. Histopathological analysis of ICC should not only be limited to the stenotic part of UPJ but also should focus on the anastomosed ends of the ureter, which reflects post-pyeloplasty outcome.

A novel compartmental approach for modeling stomach motility and gastric emptying

The stomach, a central organ in the Gastrointestinal (GI) tract, regulates the processing of ingested food through gastric motility and emptying. Understanding the stomach function is crucial for treating gastric disorders. Experimental studies in this field often face difficulties due to limitations and invasiveness of available techniques and ethical concerns. To counter this, researchers resort to computational and numerical methods. However, existing computational studies often isolate one aspect of the stomach function while neglecting the rest and employ computationally expensive methods. This paper proposes a novel cost-efficient multi-compartmental model, offering a comprehensive insight into gastric function at an organ level, thus presenting a promising alternative.The proposed approach divides the spatial geometry of the stomach into four compartments: Proximal/Middle/Terminal antrum and Pyloric sphincter. Each compartment is characterized by a set of ordinary differential equations (ODEs) with respect to time to characterize the stomach function. Electrophysiology is represented by simplified equations reflecting the “slow wave behavior” of Interstitial Cells of Cajal (ICC) and Smooth Muscle Cells (SMC) in the stomach wall. An electro-mechanical coupling model translates SMC “slow waves” into smooth muscle contractions. Muscle contractions induce peristalsis, affecting gastric fluid flow velocity and subsequent emptying when the pyloric sphincter is open. Contraction of the pyloric sphincter initiates a retrograde flow jet at the terminal antrum, modeled by a circular liquid jet flow equation.The results from the proposed model for a healthy human stomach were compared with experimental and computational studies on electrophysiology, muscle tissue mechanics, and fluid behavior during gastric emptying. These findings revealed that each “ICC” slow wave corresponded to a muscle contraction due to electro-mechanical coupling behavior. The rate of gastric emptying and mixing efficiency decreased with increasing viscosity of gastric liquid but remained relatively unchanged with gastric liquid density variations. Utilizing different ODE solvers in MATLAB, the model was solved, with ode15s demonstrating the fastest computation time, simulating 180 s of real-time stomach response in just 2.7 s. This multi-compartmental model signifies a promising advancement in understanding gastric function, providing a cost-effective and comprehensive approach to study complex interactions within the stomach and test innovative therapies like neuromodulation for treating gastric disorders.

Diabetic Gastroparesis: Epidemiology, Pathophysiology, Symptoms, and Clinical Consequences

Diabetes mellitus affects over half a billion people worldwide and is associated with numerous complications, including diabetic gastroparesis, characterized by delayed gastric emptying without mechanical obstruction. Although diabetic gastroparesis does not affect life expectancy, it significantly impairs digestion and medication absorption, complicating glucose metabolism and health management, thus reducing quality of life. The etiology of diabetic gastroparesis is multifactorial, involving autonomic neuropathy, vagus nerve dysfunction, disturbances in interstitial cells of Cajal, nitric oxide synthesis, hyperglycemia, and oxidative stress. Symptoms include early satiety, bloating, nausea, vomiting, dysphagia, and unintentional weight loss, which complicate diabetes management by causing unpredictable glycemic control. Despite advancements in understanding diabetic gastroparesis, it remains underdiagnosed due to its often asymptomatic nature. Further research is needed to elucidate its epidemiology and pathophysiology, particularly in asymptomatic patients. This review discusses the epidemiology, pathophysiology, symptoms, and clinical consequences of diabetic gastroparesis, highlighting the need for improved diagnostic and management strategies.

Exploration of the complex origins of primary constipation

Constipation is a common gastrointestinal disorder characterized by infrequent bowel movements and difficulty in passing stools. It can significantly affect an individual's quality of life and overall well-being. Understanding the causes of constipation is important for its effective management and treatment. In this paper, we have reviewed the primary causes of constipation or functional constipation. Primary constipation is a bowel disorder associated with colonic or anorectal sensorimotor or neuromuscular dysfunction. As per the literature, it is multifactorial and involves factors such as decreased interstitial cells of Cajal, altered colonic motility, enteric nervous system dysfunction, intestinal flora disturbances, and psychological influences. Clinical symptoms include difficulty in defecation, decreased frequency of defecation, or a feeling of incomplete evacuation. A comprehensive evaluation and management of constipation require an interdisciplinary approach incorporating dietary modifications, lifestyle changes, pharmacotherapy, and psychological interventions. Further research is imperative to explain the intricate mechanisms underlying constipation and develop targeted therapies for improved patient outcomes.

Interstitial cells of the sip syncytium regulate basal membrane potential in murine gastric corpus.

Smooth muscle cells (SMCs), Interstitial cells of Cajal (ICC) and Platelet-derived growth factor receptor α positive (PDGFRα+) cells form an integrated, electrical syncytium within the gastrointestinal (GI) muscular tissues known as the SIP syncytium. Immunohistochemical analysis of gastric corpus muscles showed that c-KIT+/ANO1+ ICC-IM and PDGFRα+ cells were closely apposed to one another in the same anatomical niches. We used intracellular microelectrode recording from corpus muscle bundles to characterize the roles of intramuscular ICC and PDGFRα+ cells in conditioning membrane potentials of gastric muscles. In muscle bundles, that have a relatively higher input impedance than larger muscle strips or sheets, we recorded an ongoing discharge of stochastic fluctuations in membrane potential, previously called unitary potentials or spontaneous transient depolarizations (STDs) and spontaneous transient hyperpolarizations (STHs). We reasoned that STDs should be blocked by antagonists of ANO1, the signature conductance of ICC. Activation of ANO1 has been shown to generate spontaneous transient inward currents (STICs), which are the basis for STDs. Ani9 reduced membrane noise and caused hyperpolarization, but this agent did not block the fluctuations in membrane potential quantitatively. Apamin, an antagonist of small conductance Ca2+-activated K+ channels (SK3), the signature conductance in PDGFRα+ cells, further reduced membrane noise and caused depolarization. Reversing the order of channel antagonists reversed the sequence of depolarization and hyperpolarization. These experiments show that the ongoing discharge of STDs and STHs by ICC and PDGFRα+ cells, respectively, exerts conditioning effects on membrane potentials in the SIP syncytium that would effectively regulate the excitability of SMCs.

Advancements and challenges in understanding gastrointestinal stromal tumors: A comprehensive review

The most common mesenchymal tumor affecting the gastrointestinal system is gastrointestinal stromal tumor (GIST). Although GISTs are a relatively new type of tumor, the under understanding of these tumors has increased quickly. Nevertheless, there is a dearth of research on this illness in India, and the majority of treatment plans are based on studies performed on populations outside of the nation. Since the 1990s, considerable progress has been made in our knowledge of the lineage of origin of the GIST domain. According to recent research, multipotent mesenchymal stem cells are the source of GISTs, which are thought to occur in 10-20 cases per million people annually. With the overexpression of the tyrosine kinase receptor KIT in intestinal Cajal cells, GISTs are the most prevalent malignant subepithelial lesions (SELs) in the digestive tract. GISTs can have a variety of morphologies, such as rhabdomyosarcoma, angiosarcoma, or undifferentiated pleomorphic sarcoma, which makes diagnosis difficult. However, new developments in molecular targeted therapy have transformed solid tumor oncology and provided exciting new avenues for treatment. To differentiate dedifferentiated GISTs from other gastrointestinal malignancies, this review paper will address current immunohistochemical markers and provide an outline of the morphologic and molecular features of these tumors. The findings also emphasize the importance of GIST genetic testing, progressive surgical approaches, adjuvant and neoadjuvant therapy for localized disorders, and metastatic condition-addressing methodologies. This article's major body explores the impact of imatinib therapy, the rarity of GISTs in pediatric patients, imaging methods for staging and monitoring, and difficulties with treating anorectal GISTs. This study highlights how crucial it is to pinpoint particular molecular subtypes to inform therapeutic choices for adjuvant and metastatic therapies.

Metastatic GIST with a TWIST of RCC: A case report

Gastrointestinal Stromal Tumors (GIST) is a tumor of mesenchymal origin in the digestive tract, arising from Interstitial cells of Cajal. Majorly, they are an incidental finding in people of older age group (&amp;#62;60 years) with very rare bone metastasis. Our aim is to understand the role of genetic mutations in metastasis of GIST and coexistence of other malignancy in the same patient. We present an unusual case of a 75-year-old male with jejunal GIST, managed with resection of the tumor and imatinib, who 15 years later presented with subsequent liver, rare femoral head metastases and coexisting Renal Cell Carcinoma in left kidney. GIST cases can be associated with different syndromes and malignancies. This necessitates additional work up and long term follow up.

Understanding Gastric GIST: From Pathophysiology to Personalized Treatment.

Background: Gastric gastrointestinal stromal tumors (GISTs) represent a subset of gastrointestinal tumors predominantly found in the stomach. Despite their rarity, these tumors carry significant implications for patient health and management. GISTs are potentially malignant tumors with unpredictable progression. They originate from the interstitial cells of Cajal, which are positioned between the intramural neurons and the smooth muscle cells of the digestive tract. These tumors are characterized primarily by mutations in the c-Kit gene, as well as other mutations such as those in the platelet-derived growth factor receptor alpha (PDGFRA) gene. Methods: Our comprehensive search across five databases initially yielded 2976 articles. After eliminating 197 duplicates, we screened the titles and abstracts of 2779 articles, excluding 2692 for not meeting the inclusion criteria. During the full-text screening, 16 more articles were excluded. Ultimately, 71 papers met the inclusion criteria and were included in our analysis. Results: Due to differences in study designs, inclusion criteria for patients, and reported outcomes, a meta-analysis was not conducted. The accurate diagnosis of GIST is established through histopathological examination and immunohistochemistry. Histopathologically, GISTs are classified into three main types: spindle cell, epithelioid, and mixed. The therapeutic management of GIST involves surgery, endoscopic treatment, and chemotherapy. Conclusions: The prognosis for GIST patients depends on various factors, including risk category, disease stage, applied treatments, and recurrence post-treatment. A significant recent advancement comes from artificial intelligence, which can be increasingly involved in both the diagnosis and treatment of this tumor.

Assessment of Changes in the Function of Interstitial Cells of Cajal and Fecundity During Chronic Salpingitis: An Experimental Study

Assessment of Changes in the Function of Interstitial Cells of Cajal and Fecundity During Chronic Salpingitis: An Experimental Study