Citations

AbstractBackgroundScleroderma, also referred to as systemic sclerosis, is a multifaceted autoimmune condition characterized by abnormal fibrosis and impaired vascular function. Pathologically, it encompasses the persistent presence of inflammation, abnormal collagen buildup, and restructuring of blood vessels in various organs, resulting in a wide range of clinical symptoms. This review incorporates the most recent scientific literature on scleroderma, with a particular emphasis on its pathophysiology, clinical manifestations, diagnostic approaches, and treatment options.MethodologyA comprehensive investigation was carried out on numerous databases, such as PubMed, MEDLINE, Scopus, Web of Science, and Google Scholar, to collect pertinent studies covering diverse facets of scleroderma research.ResultsScleroderma presents with a range of systemic manifestations, such as interstitial lung disease, gastrointestinal dysmotility, Raynaud's phenomenon, pulmonary arterial hypertension, renal complications, neurological symptoms, and cardiac abnormalities. Serological markers, such as antinuclear antibodies, anti‐centromere antibodies, and anti‐topoisomerase antibodies, are important for classifying diseases and predicting their outcomes.DiscussionThe precise identification of scleroderma is crucial for promptly and correctly implementing effective treatment plans. Treatment approaches aim to improve symptoms, reduce complications, and slow down the progression of the disease. An integrated approach that combines pharmacological agents, including immunosuppressants, endothelin receptor antagonists, and prostanoids, with nonpharmacological interventions such as physical and occupational therapy is essential for maximizing patient care.ConclusionThrough the clarification of existing gaps in knowledge and identification of emerging trends, our goal is to improve the accuracy of diagnosis, enhance the effectiveness of therapeutic interventions, and ultimately enhance the overall quality of life for individuals suffering from scleroderma. Ongoing cooperation and creative research are necessary to advance the field and achieve improved patient outcomes and new therapeutic discoveries.

Juvenile multiple sclerosis (JMS) is a rare but significant subtype of multiple sclerosis (MS) that affects a small percentage of patients under the age of 10 and 3–5% of all MS patients. Despite its rarity, JMS poses unique challenges in terms of diagnosis, treatment, and management, as it can significantly impact a child or adolescent’s physical, cognitive, and emotional development. JMS presents with a varying spectrum of signs and symptoms such as coordination difficulties and permanent cognitive dysfunctions and may include atypical clinical features such as seizures, acute disseminated encephalomyelitis, and optic neuritis, making diagnostic evaluations challenging. Whilst the biology of JMS shares similarities with adult-onset MS, there exist notable distinctions in disease progression, clinical manifestations, and ultimate prognoses. The International Pediatric MS Study Group (IPMSSG) was founded in 2005 to improve understanding of JMS, but there remains a lack of knowledge and guidelines on the management of this condition. This review summarizes the current knowledge on JMS, including its epidemiology, clinical presentations, diagnostic challenges, current treatment options, and outcomes. Current treatment options for JMS include disease-modifying therapies, but JMS can also result in impaired quality of life and psychiatric comorbidity, highlighting the need for comprehensive care for affected children. Through gathering and analyzing scattered studies and recent updates on JMS, the authors aim to address the gaps in current knowledge on JMS and provide an improved understanding of appropriate care for affected children. By doing so, this review hopes to contribute to improving the quality of life and outcomes for JMS patients.

Multiple sclerosis (MS) is a chronic inflammatory disease that damages the myelin sheath around the axons of the central nervous system. While there are periods of inflammation and remyelination in MS, the latter can sometimes be insufficient and lead to the formation of lesions in the brain and spinal cord. Environmental factors such as vitamin D deficiency, viral or bacterial infections, tobacco smoking, and anxiety have been shown to play a role in the development of MS. Dysbiosis, where the composition of the microbiome changes, may also be involved in the pathogenesis of MS by affecting the gut’s microbial population and negatively impacting the integrity of the epithelia. While the cause of MS remains unknown, genetic susceptibility, and immunological dysregulation are believed to play a key role in the development of the disease. Further research is needed to fully understand the complex interplay between genetic, environmental, and microbial factors in the pathogenesis of MS.

Dysfunction in the epithelium, breakdown of the blood–brain barrier, and consequent leukocyte and T-cell infiltration into the central nervous system define Vascular Multiple Sclerosis. Multiple sclerosis (MS) affects around 2.5 million individuals worldwide, is the leading cause of neurological impairment in young adults, and can have a variety of progressions and consequences. Despite significant discoveries in immunology and molecular biology, the root cause of MS is still not fully understood, as do the immunological triggers and causative pathways. Recent research into vascular anomalies associated with MS suggests that a vascular component may be pivotal to the etiology of MS, and there can be actually a completely new entity in the already available classification of MS, which can be called ‘vascular multiple sclerosis’. Unlike the usual other causes of MS, vascular MS is not dependent on autoimmune pathophysiologic mechanisms, instead, it is caused due to the blood vessels pathology. This review aims to thoroughly analyze existing information and updates about the scattered available findings of genetics, pro-angiogenetic factors, and vascular abnormalities in this important spectrum, the vascular facets of MS.

The association and interaction between the central nervous system (CNS) and enteric nervous system (ENS) is well established. Essentially ENS is the second brain, as we call it. We tried to understand the structure and function, to throw light on the functional aspect of neurons, and address various disease manifestations. We summarized how various neurological disorders influence the gut via the enteric nervous system and/or bring anatomical or physiological changes in the enteric nervous system or the gut and vice versa. It is known that stress has an effect on Gastrointestinal (GI) motility and causes mucosal erosions. In our literature review, we found that stress can also affect sensory perception in the central nervous system. Interestingly, we found that mutations in the neurohormone, serotonin (5-HT), would result in dysfunctional organ development and further affect mood and behavior. We focused on the developmental aspects of neurons and cognition and their relation to nutritional absorption via the gastrointestinal tract, the development of neurodegenerative disorders in relation to the alteration in gut microbiota, and contrariwise associations between CNS disorders and ENS. This paper further summarizes the synergetic relation between gastrointestinal and neuropsychological manifestations and emphasizes the need to include behavioral therapies in management plans.

Multiple sclerosis (MS) and myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) share the symptom of fatigue, and might even coexist together. Specifically focusing on genetics, pathophysiology, and neuroimaging data, the authors discuss an overview of the parallels, correlation, and differences in fatigue between MS and ME/CFS along with ME/CFS presence in MS. Studies have revealed that the prefrontal cortex and basal ganglia regions, which are involved in fatigue regulation, have similar neuroimaging findings in the brains of people with both MS and ME/CFS. Additionally, in both conditions, genetic factors have been implicated, with particular genes known to enhance susceptibility to MS and CFS. Management approaches for fatigue in MS and ME/CFS differ based on the underlying factors contributing to fatigue. The authors also focus on the recent updates and the relationship between MS and sleep disorders, including restless legs syndrome, focusing on pathophysiology and therapeutic approaches. Latest therapeutic approaches like supervised physical activity and moderate-intensity exercises have shown better outcomes.

Pancreatic carcinoma (Ca Pancreas) is the third leading cause of cancer-related deaths in the world. The malignancies of the pancreas can be diagnosed with the help of various imaging modalities. An endoscopic ultrasound with a tissue biopsy is so far considered to be the gold standard in terms of the detection of Ca Pancreas, especially for lesions <2 mm. However, other methods, like computed tomography (CT), ultrasound, and magnetic resonance imaging (MRI), are also conventionally used. Moreover, newer techniques, like proteomics, radiomics, metabolomics, and artificial intelligence (AI), are slowly being introduced for diagnosing pancreatic cancer. Regardless, it is still a challenge to diagnose pancreatic carcinoma non-invasively at an early stage due to its delayed presentation. Similarly, this also makes it difficult to demonstrate an association between Ca Pancreas and other vital organs of the body, such as the heart. A number of studies have proven a correlation between the heart and pancreatic cancer. The tumor of the pancreas affects the heart at the physiological, as well as the molecular, level. An overexpression of the SMAD4 gene; a disruption in biomolecules, such as IGF, MAPK, and ApoE; and increased CA19-9 markers are a few of the many factors that are noted to affect cardiovascular systems with pancreatic malignancies. A comprehensive review of this correlation will aid researchers in conducting studies to help establish a definite relation between the two organs and discover ways to use it for the early detection of Ca Pancreas.

AbstractBackgroundPrimary‐progressive multiple sclerosis (PPMS) and relapsing‐remitting multiple sclerosis (RRMS) are two frequent multiple sclerosis (MS) subtypes that involve 10%–15% of patients. PPMS progresses slowly and is diagnosed later in life. Both subtypes are influenced by genetic and environmental factors such as smoking, obesity, and vitamin D insufficiency. Although there is no cure, ocrelizumab can reduce symptoms and delay disease development. RRMS is an autoimmune disease that causes inflammation, demyelination, and disability. Early detection, therapy, and lifestyle changes are critical. This study delves into genetics, immunology, biomarkers, neuroimaging, and the usefulness of ocrelizumab in the treatment of refractory patients of PPMS.MethodIn search of published literature providing up‐to‐date information on PPMS and RRMS, this review conducted numerous searches in databases such as PubMed, Google Scholar, MEDLINE, and Scopus. We looked into genetics, immunology, biomarkers, current breakthroughs in neuroimaging, and the role of ocrelizumab in refractory cases.ResultsOur comprehensive analysis found considerable advances in genetics, immunology, biomarkers, neuroimaging, and the efficacy of ocrelizumab in the treatment of refractory patients.ConclusionEarly detection, timely intervention, and the adoption of lifestyle modifications play pivotal roles in enhancing treatment outcomes. Notably, ocrelizumab has demonstrated potential in symptom control and mitigating the rate of disease advancement, further underscoring its clinical significance in the management of MS.

Abstract Optical coherence tomography (OCT) is an advanced imaging modality to detect Barrett’s esophagus (BE) dysplasia, providing widefield, cross-sectional imaging and microscopic resolution. BE dysplasia is characterized under OCT by the presence and number of glandular structures with atypical morphology. Accurate detection and interpretation of BE glands under OCT is essential to detect dysplastic lesions. Object Detection using deep learning has the potential to identify glands from OCT images. We developed a YOLO model to identify the presence of glands in BE tissue. The YOLOv4 object detector was trained on a custom BE dataset of 30 patients with confirmed BE who underwent OCT imaging, of which 222 OCT images included at least one gland. Our model identified glands with a high average precision of 88.79% on the test dataset. We showed that the developed model is robust to rotation, brightness, and blur in images. We have implemented an object detection model to identify glands from OCT images with promising results accurately. This model has the potential to improve the diagnosis and surveillance of BE by eliminating human error and missed dysplastic lesions adaptable for capsule endoscopy applications.