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.

Renal cell carcinoma (RCC) represents 85–95% of kidney cancers and is the most frequent type of renal cancer in adult patients. It accounts for 3% of all cancer cases and is in 7th place among the most frequent histological types of cancer. Clear cell renal cell carcinoma (ccRCC), accounts for 75% of RCCs and has the most kidney cancer-related deaths. One-third of the patients with ccRCC develop metastases. Renal cancer presents cellular alterations in sugars, lipids, amino acids, and nucleic acid metabolism. RCC is characterized by several metabolic dysregulations including oxygen sensing (VHL/HIF pathway), glucose transporters (GLUT 1 and GLUT 4) energy sensing, and energy nutrient sensing cascade. Metabolic reprogramming represents an important characteristic of the cancer cells to survive in nutrient and oxygen-deprived environments, to proliferate and metastasize in different body sites. The phosphoinositide 3-kinase-AKT-mammalian target of the rapamycin (PI3K/AKT/mTOR) signaling pathway is usually dysregulated in various cancer types including renal cancer. This molecular pathway is frequently correlated with tumor growth and survival. The main aim of this review is to present renal cancer types, dysregulation of PI3K/AKT/mTOR signaling pathway members, crosstalk with VHL/HIF axis, and carbohydrates, lipids, and amino acid alterations.

Since we aim to test new options to find medication for cognitive disorders, we have begun to assess the effect of semaglutide and to conduct a review gathering studies that have attempted this purpose. This systematic review focuses on the cognitive effects of semaglutide, a glucagon-like peptide 1 receptor agonist (GLP-1 RA), in the context of neurological and cognitive impairment. Semaglutide, a synthetic GLP-1 analog, showcased neuroprotective effects beyond metabolic regulation. It mitigated apoptosis and improved cognitive dysfunction in cerebrovascular disease, suggesting broader implications for neurological well-being. Also, studies highlighted GLP-1 RAs’ positive impact on olfactory function in obese individuals with type 2 diabetes, on neurodegenerative disorders, multiple sclerosis, and endotoxemia. In order to analyze current studies that assess the impact of semaglutide on cognitive function, a literature search was conducted up to February 2024 on two online databases, MEDLINE (via PubMed) and Web of Science Core Collection, as well as various websites. Fifteen studies on mice populations and two studies on cell lines were included, analyzed, and assessed with bias-specific tools. The neuroprotective and anti-apoptotic properties of GLP-1 and its analogs were emphasized, with animal models and cell line studies demonstrating enhanced cognitive function. While promising, limitations include fewer studies, highlighting the need for extensive research, particularly in the human population. Even though this medication seems promising, there are significant limitations, one of which is the lack of studies on human subjects. Therefore, this review aims to gather current evidence.

(1) Background: Chronic kidney disease (CKD), as well as antimicrobial resistance (AMR) represent major global health problems, with important social and economic implications. It was reported that CKD is a risk factor for antimicrobial resistance, but evidence is scarce. In addition, CKD is recognized to be a risk factor for complicated urinary tract infections (UTIs). (2) Methods: We conducted an observational study on 564 adult in-hospital patients diagnosed with urinary tract infections. The aim of the study was to identify the risk factors for AMR, as well as multiple drug resistance (MDR) and the implicated resistance patterns. (3) Results: The mean age was 68.63 ± 17.2 years. The most frequently isolated uropathogens were Escherichia coli strains (68.3%) followed by Klebsiella species (spp. (11.2%). In 307 cases (54.4%)), the UTIs were determined by antibiotic-resistant bacteria (ARBs) and 169 cases (30%) were UTIs with MDR strains. Increased age (≥65) OR 2.156 (95% CI: 1.404–3.311), upper urinary tract obstruction OR 1.666 (1.083–2.564), indwelling urinary catheters OR 6.066 (3.919–9.390), chronic kidney disease OR 2.696 (1.832–3.969), chronic hemodialysis OR 4.955 (1.828–13.435) and active malignancies OR 1.962 (1.087–3.540) were independent risk factors for MDR UTIs. In a multivariate logistic regression model, only indwelling urinary catheters (OR 5.388, 95% CI: 3.294–8.814, p < 0.001), CKD (OR 1.779, 95% CI: 1.153–2.745, p = 0.009) and chronic hemodialysis (OR 4.068, 95% 1.413–11.715, p = 0.009) were risk factors for UTIs caused by MDR uropathogens. (4) Conclusions: CKD is an important risk factor for overall antimicrobial resistance, but also for multiple-drug resistance.

Worldwide, urinary tract infections (UTIs) have an increased incidence, especially in women. Recurrent UTIs (rUTIs) appear in less than three months in 80% of the cases, being associated with age, sexual activity, or diabetes mellitus. Antibiotics represent the first line of treatment for rUTIs after the diagnosis based on a positive mid-stream urine (MSU) culture. Alternative therapies including low-dose antibiotic treatment, immunoprophylaxis, cranberry extracts, probiotics, D-mannose, intravesical instillations, methenamine, and estrogens may reduce the recurrence of UTIs in female patients. Multimodal therapy seems to be the future in preventing and treating rUTIs. The main aim of this narrative review is to present the actual therapeutic challenges and the most efficient prophylaxis options in women diagnosed with rUTIs.

Background and Objectives: The main cause of morbidity and mortality in hemodialysis patients is cardiovascular disease, which is quite common. The main objective of our study was to investigate the relationship between oxidative stress, inflammation, and vascular and valvular calcifications in hemodialysis patients. Materials and Methods: This observational study had 54 hemodialysis patients, with an average age of 60.46 ± 13.18 years. Cardiovascular ultrasound was used to detect and/or measure aortic and mitral valve calcifications, carotid and femoral atheroma plaques, and common carotid intima-media thickness. The aortic calcification score was determined using a lateral abdomen plain radiograph. The inflammatory, oxidative, metabolic, and dietary statuses, as well as demographic characteristics, were identified. Results: There were significant correlations between the levels of IL-6 and carotid plaque number (p = 0.003), fibrinogen level and aortic valve calcifications (p = 0.05), intima-media thickness (p = 0.0007), carotid plaque number (p = 0.035), femoral plaque number (p = 0.00014), and aortic calcifications score (p = 0.0079). Aortic annulus calcifications (p = 0.03) and intima-media thickness (p = 0.038) were adversely linked with TNF-α. Nutrition parameters were negatively correlated with atherosclerosis markers: number of carotid plaques with albumin (p = 0.013), body mass index (p = 0.039), and triglycerides (p = 0.021); number of femoral plaques with phosphorus (0.013), aortic calcifications score with albumin (p = 0.051), intima-media thickness with LDL-cholesterol (p = 0.042). Age and the quantity of carotid plaques, femoral plaques, and aortic calcifications were linked with each other (p = 0.0022, 0.00011, and 0.036, respectively). Aortic annulus calcifications (p = 0.011), aortic valve calcifications (p = 0.023), and mitral valve calcifications (p = 0.018) were all associated with an increased risk of death. Conclusions: Imaging measures of atherosclerosis are adversely connected with dietary status and positively correlated with markers of inflammation and risk of mortality.