Mucocles of the appendix, encompassing mucinous cystadenomas and mucinous cystadenocarcinomas, represent rare but clinically significant appendiceal lesions characterized by the accumulation of mucin within the appendix lumen. This review explores the diagnostic complexities and treatment strategies associated with mucocles, emphasizing the importance of its accurate recognition and management. Diagnostic challenges arise due to overlapping symptoms with acute appendicitis and other appendiceal pathologies, necessitating a multidimensional approach that includes imaging, histopathological analysis, and clinical correlation. Treatment options range from appendectomy for benign lesions to more extensive surgical procedures, such as right hemicolectomy for malignant forms. Prognostic factors, including histological subtype and tumor size, influence treatment decisions and long-term outcomes. By synthesizing current evidence and clinical insights, this review aims to provide a comprehensive framework for clinicians to navigate the complexities of mucocles of the appendix, offering perspectives that can guide effective management and future research endeavors.

Follicular thyroid carcinoma (FTC) is the second most common type of thyroid cancer, presenting unique diagnostic and therapeutic challenges. This review provides a comprehensive analysis of the recent advancements in the diagnosis and treatment of FTC, emphasizing the significance of these developments in improving patient outcomes. We discuss the evolution of diagnostic techniques, including advancements in imaging modalities, fine needle aspiration biopsy, and molecular diagnostics, which have enhanced the accuracy of FTC detection and differentiation from benign conditions. The review also evaluates current treatment strategies, including surgical interventions, radioactive iodine therapy, and targeted therapies, examining their effectiveness and impact on patient prognosis. Additionally, we address ongoing challenges in FTC management, such as variability in treatment guidelines and disparities in care. Finally, the review explores emerging therapies and future research directions, highlighting innovations that may further optimize FTC management. By synthesizing current knowledge and identifying future research opportunities, this review aims to contribute to refining diagnostic and therapeutic approaches for FTC.

Multiple sclerosis (MS) is a heterogenous autoimmune-mediated disease of the central nervous system (CNS) characterized by inflammation, demyelination and chronic progressive neurodegeneration. Among its broad and unpredictable range of neuropsychiatric symptoms, behavioral changes are common, even from the early stages of the disease, while they are associated with cognitive deficits in advanced MS. According to DSM-5, behavioral disorders include attention deficits, oppositional, defiant and conduct disorders, anxiety, panic, obsessive-compulsive disorders (OCD), disruptive and emotional disorders, while others include also irritability, agitation, aggression and executive dysfunctions. Approximately 30 to 80% of individuals with MS demonstrate behavioral changes associated with disease progression. They are often combined with depression and other neuropsychiatric disorders, but usually not correlated with motor deficits, suggesting different pathomechanisms. These and other alterations contribute to disability in MS. While no specific neuropathological data for behavioral changes in MS are available, those in demyelination animal models share similarities with white matter and neuroinflammatory abnormalities in humans. Neuroimaging revealed prefrontal cortical atrophy, interhemispheric inhibition and disruption of fronto-striato-thalamic and frontoparietal networks. This indicates multi-regional patterns of cerebral disturbances within the MS pathology although their pathogenic mechanisms await further elucidation. Benefits of social, psychological, behavioral interventions and exercise were reported. Based on systematical analysis of PubMed, Google Scholar and Cochrane library, current epidemiological, clinical, neuroimaging and pathogenetic evidence are reviewed that may aid early identification of behavioral symptoms in MS, and promote new therapeutic targets and strategies.

Secondary BRAF variations have been identified as a mechanism of resistance to tyrosine kinase inhibitors (TKIs) in patients with driver gene-positive NSCLC. Nevertheless, there is still a lack of consensus regarding the characteristics and subsequent treatment strategies for these patients. We retrospectively reviewed the medical records of patients with driver gene-positive NSCLC who received TKIs therapy at Zhejiang Cancer Hospital between May 2016 and December 2023. The clinical and genetic characteristics of these patients were assessed, along with the impact of various treatment strategies on survival. This study enrolled 27 patients with advanced NSCLC, in whom BRAF variations occurred at a median time of 28 months after the initiation of targeted therapy. The multivariate accelerated failure time (AFT) model revealed that, compared to chemotherapy-based regimens group, the combined targeted therapy group (p < 0.001) and the combined local treatment group for oligo-progression (p < 0.001) significantly extended patient survival. In contrast, continuing the original signaling pathway\'s targeted monotherapy was associated with shorter survival (p = 0.034). The median global OS for each treatment group was as follows: chemotherapy-based regimens group, 45 months; combined targeted therapy group, 59 months; combined local treatment group for patients with oligo-progression, 46 months; and targeted monotherapy group, 36 months. Study results indicate that the combination targeted therapy group (including TKIs, BRAF inhibitors, and/or MEK inhibitors) and the localized treatment group are more effective than traditional chemotherapy-based regimens in improving survival. Additionally, continuing targeted monotherapy along the original signaling pathway proves less effective than chemotherapy-based regimens.

This review explores the connection between the ocular surface microbiome and glaucoma, highlighting its impact on disease progression. Beginning with an overview of global glaucoma significance, it emphasizes the importance of understanding the cellular characteristics and microbiology of the ocular microbiome. A search was conducted on the PubMed and Cochrane Library databases using the phrase \"ocular microbiome glaucoma\". 0 records were returned from the Cochrane Library while 21 were returned from PubMed. A total of 21 results were retrieved from 2017 to 2024. This comprised one opinion paper, four original research articles, and 16 reviews. This review covered the anatomy of the ocular surface, advanced analysis methods, and the ocular microbiome. It also delved into dysbiosis in glaucoma, addressing altered microbial communities and their potential role in disease progression. The intricate interplay between the ocular microbiome and the host\'s immune system is explored, emphasizing crosstalk and inflammatory responses. The review concludes by discussing therapeutic implications, including modulating ocular microbiota and potential future treatment strategies. Understanding the microbiome in healthy and glaucomatous eyes can help researchers and clinicians in innovative approaches to ocular health.

Multiple sclerosis (MS) is a chronic autoimmune disease characterized by pathological processes of demyelination, subsequent axonal loss, and neurodegeneration within the central nervous system. Despite the availability of numerous disease-modifying therapies that effectively manage this condition, there is an emerging need to identify novel therapeutic targets, particularly for progressive forms of MS. Based on contemporary insights into disease pathophysiology, ongoing efforts are directed toward developing innovative treatment modalities. Primarily, monoclonal antibodies have been extensively investigated for their efficacy in influencing specific pathological pathways not yet targeted. Emerging approaches emphasizing cellular mechanisms, such as chimeric antigen receptor T cell therapy targeting immunological cells, are attracting increasing interest. The evolving understanding of microglia and the involvement of ferroptotic mechanisms in MS pathogenesis presents further avenues for targeted therapies. Moreover, innovative treatment strategies extend beyond conventional approaches to encompass interventions that target alterations in microbiota composition and dietary modifications. These adjunctive therapies hold promise as complementary methods for the holistic management of MS. This narrative review aims to summarize current therapies and outline potential treatment methods for individuals with MS.

Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related deaths worldwide. Dendritic cells (DCs) constitute a heterogeneous group of antigen-presenting cells that are important for initiating and regulating both innate and adaptive immune responses. As a crucial component of the immune system, DCs have a pivotal role in the pathogenesis and clinical treatment of CRC. DCs cross-present tumor-related antigens to activate T cells and trigger an antitumor immune response. However, the antitumor immune function of DCs is impaired and immune tolerance is promoted due to the presence of the tumor microenvironment. This review systematically elucidates the specific characteristics and functions of different DC subsets, as well as the role that DCs play in the immune response and tolerance within the CRC microenvironment. Moreover, how DCs contribute to the progression of CRC and potential therapies to enhance antitumor immunity on the basis of existing data are also discussed, which will provide new perspectives and approaches for immunotherapy in patients with CRC.

BACKGROUND: Trigeminal neuralgia (TN), marked by chronic pain from neural damage, is closely associated with inflammation. The role of OTULIN, a key regulator in inflammation and autophagy, is not fully understood in TN. The regulatory mechanism of OTULIN, a key protein involved in modulating inflammatory responses and autophagy processes, remains incompletely elucidated, particularly in the context of TN and neuroinflammation.
METHODS: An infraorbital nerve ligation-induced rat model of TN was used. OTULIN\'s expression was modulated using adenovirus vectors and short hairpin RNA. The impact on pain and inflammatory responses was assessed via quantitative real-time polymerase chain reaction, western blot, immunofluorescence, and transcriptomic analysis.
RESULTS: Enhanced OTULIN expression significantly increased head withdrawal thresholds and reduced pain sensitivity and neuroinflammatory markers in the model. Conversely, silencing OTULIN exacerbated pain and inflammation. Transcriptomic data revealed OTULINs influence on both inflammatory and autophagy pathways, specifically in suppressing NLR family pyrin domain containing 3 (NLRP3) inflammasome and promoting autophagy. In vitro experiments demonstrated OTULIN\'s inhibition of inflammatory markers in microglia and neurons.
CONCLUSIONS: OTULIN is crucial in modulating TN, reducing neuropathic pain and neuroinflammation by activating the autophagy pathway and inhibiting the NLRP3 inflammasome.

Calpain, a key member of the Calpain cysteine protease superfamily, performs limited protein hydrolysis in a calcium-dependent manner. Its activity is tightly regulated due to the potential for non-specific cleavage of various intracellular proteins upon aberrant activation. A thorough review of the literature from 2010 to 2023 reveals 121 references discussing cardiovascular and cerebrovascular diseases. Dysregulation of the Calpain system is associated with various pathological phenomena, including lipid metabolism disorders, inflammation, apoptosis, and excitotoxicity. Although recent studies have revealed the significant role of Calpain in cardiovascular and cerebrovascular diseases, the precise mechanisms remain incompletely understood. Exploring the potential of Calpain inhibition as a therapeutic approach for the treatment of cardiovascular and cerebrovascular diseases may emerge as a compelling area of interest for future calpain research.

Hepatocellular adenoma (HCA) is an uncommon benign liver tumor that exhibits a variety of subtypes, each distinguished by unique molecular alterations. This case report describes a 43-year-old man with a history of alcoholism who presented with stomach pain. Imaging revealed multiple hepatic lesions and sigmoid colon inflammation, while laboratory tests showed mild neutrophilic leukocytosis and elevated liver enzymes. Tumor markers were normal. A liver biopsy confirmed HCA with hepatocyte nuclear factor-1 alpha (HNF-1α) inactivation, characterized by negative immunostaining for glutamine synthetase, nuclear beta-catenin, serum amyloid A, C-reactive protein, and liver fatty acid-binding protein (L-FABP). This case is unique due to the patient\'s gender and the absence of typical risk factors such as abnormal hormone levels. HCAs in males, particularly with HNF-1α inactivation, are rare and pose diagnostic challenges. Comprehensive diagnostic approaches, including biopsy and immunohistochemical analysis, are crucial for accurate subtype identification. The potential for malignant transformation, particularly in male patients, underscores the need for vigilant monitoring and appropriate management. This case highlights the importance of considering HCA in differential diagnoses regardless of gender and typical risk factors, contributing valuable insights into the diverse presentations and risks associated with HCA, and emphasizing the need for awareness and further research to improve diagnosis and management of this rare condition.