Gastric cancer (GC) is the fourth leading cause of death worldwide, with more than 1 million cases diagnosed every year. Helicobacter pylori represents the main risk factor, being responsible for 78% of the cases. Increased amounts of salt, pickled food, red meat, alcohol, smoked food, and refined sugars negatively affect the stomach wall, contributing to GC development. Several gene mutations, including PIK3CA, TP53, ARID1A, CDH1, Ras, Raf, and ERBB3 are encountered in GC pathogenesis, leading to phosphatidylinositol 3-kinase (PI3K) protein kinase B (AKT)/mammalian target of rapamycin (mTOR)—PI3K/AKT/mTOR—and mitogen-activated protein kinase (MAPK) signaling pathway activation and promoting tumoral activity. Helicobacter pylori, growth factors, cytokines, hormones, and oxidative stress also activate both pathways, enhancing GC development. In clinical trials, promising results have come from monoclonal antibodies such as trastuzumab and ramucirumab. Dual inhibitors targeting the PI3K/AKT/mTOR and MAPK signaling pathways were used in vitro studies, also with promising results. The main aim of this review is to present GC incidence and risk factors and the dysregulations of the two protein kinase complexes together with their specific inhibitors.

Background/Objectives: This study explores the micro-structure of celiac ganglia using two-photon microscopy (TPM) to highlight histological features in neurodegenerative conditions. Neurodegenerative diseases like Parkinson’s disease (PD) are linked to dysautonomia, impacting autonomic regulation and leading to significant gastrointestinal and autonomic symptoms. Our research compares imaging results from TPM and SHG microscopy, visualizing neuronal integrity, collagen distribution, and the architectural organization of celiac ganglia. SHG specifically allows detailed imaging of collagen fibers and neuronal structures, revealing alterations in collagen density and organization that correlate with dysautonomia. Methods: The cross-sectional study was conducted at “Dr. Carol Davila” Central Military Emergency University Hospital, Bucharest, Romania, involving 70 participants diagnosed with PD (Hoehn and Yahr stages 2–4), including 35 with dysautonomia and 35 without. We utilized samples from PD patients with and without dysautonomia, applying immunohistochemical markers for sympathetic neurons. Results: Our findings reveal significant pathological changes in neuronal structure and collagen architecture. Immunohistochemical markers (neuropeptide Y, neurofilament heavy chain (NF-H), and tyrosine hydroxylase) were employed to characterize sympathetic neurons, while TPM and SHG provided high-resolution imaging of neuronal integrity and extracellular matrix composition. Conclusions: These imaging techniques present a promising tool for early diagnosis and assessment of neurodegeneration and dysautonomia in PD patients. Moreover, these techniques may represent a critical bridge between histopathological findings and clinical manifestations, underscoring their role in enhancing our understanding of neurodegeneration and autonomic dysfunction in Parkinson’s disease.

Dysautonomia, a parasympathetic-sympathetic imbalance, has clinical and public health consequences. Colon neoplasm is linked to dysautonomia through a

The celiac ganglia are a network of nerve fibers that regulate various functions related to digestion, while the celiac trunk is a major artery that