Gastrointestinal endoscopy has undergone significant transformation since its first introduction in the early 20th century. Despite advances in modern endoscopy, its precision in detecting and removing colorectal cancer (CRC) varies; colorectal polyps or cancer are still missed in 2.1-5.9% of cases. Additionally, post-colonoscopy CRC occurs in 30% of patients who have undergone incomplete polyp resection. When biopsies are taken, only 11.4% are found to be malignant, rendering 88.6% of tissue removal unnecessary. To address these shortcomings, modern endoscopy is evolving. Current endoscopic modalities include wide-field and microscopic-field endoscopy. Wide-field view endoscopy remains the most frequently used type and includes the current standard of practice—white light endoscopy—as well as other modalities such as virtual and dye-based chromoendoscopy, ultrathin endoscopy, and capsule endoscopy. Microscopic field endoscopy encompasses several new emerging modalities that can provide microscopic resolution capable of diagnosing lesions in vivo (optical biopsy), thus reducing the number of unnecessary biopsies. However, the emerging technology comes with a learning curve and requires time for endoscopists to master and achieve interobserver agreement. Consequently, there is a growing opportunity to develop machine learning technology to assist with the learning process. We review current modalities available for the diagnosis of CRC, including the current standard of practice, new enhanced imaging modalities, and optical biopsy.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is currently a pressing public health issue associated with adverse outcomes such as cirrhosis, malignancy, transplantation, and mortality. Lifestyle modifications constitute the most effective and fundamental management approach, but they often pose challenges in sustaining long-term clinical benefits. Hence, there is a critical need to enhance our understanding through pharmacological management, which unfortunately remains limited. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as a leading treatment in the fields of diabetes and obesity, with recent preclinical and clinical studies indicating significant benefits in the management and treatment of MASLD. Our article begins by reviewing the beneficial therapeutic components of GLP-1RAs in MASLD. Subsequently, from a clinical research perspective, we concluded with the liver outcomes of current primary GLP-1RAs and co-agonists. Finally, we presented our insights on clinical concerns such as appropriate trial endpoints, management of comorbidities, and future developments. In conclusion, the benefits of GLP-1RAs in MASLD are promising, and background therapy involving metabolic modulation may represent one of the future therapeutic paradigms.

Obesity has become a global epidemic affecting diverse populations and leading to metabolic syndrome across different sexes and age groups. A significant aspect of obesity is the development of leptin resistance, primarily due to the inefficient transport of leptin across the blood-brain barrier and other mechanisms such as protein folding and dysregulation of leptin signaling in brain areas related to energy and adipose tissue metabolism. This hindrance in leptin delivery poses a challenge to using this adipokine as a potential therapy for obesity. Current research focuses on understanding the complex molecular pathways that link diet-induced obesity, characterized by increased levels of leptin, to the onset of metabolic syndrome. This syndrome encompasses various health issues, including type 2 diabetes mellitus, and involves intricate mechanisms primarily affecting pancreatic β-cells. This bioinformatics-assisted review describes key biological elements of known pathways, such as the forkhead box protein O1/leptin receptor and Janus kinase/signal transducer and activator of transcription 3, and discusses future directions that might contribute to understanding the relationship between obesity, leptin resistance, and metabolic complications (e.g., Rac1/cell division control protein 42 homolog), paving the way for future research on targeted therapeutic interventions.

The role of platelet autophagy in cirrhotic thrombocytopenia (CTP) remains unclear. This study aimed to investigate the impact of platelet autophagy in CTP and elucidate the regulatory mechanism of hydrogen sulfide (H2S) on platelet autophagy.

Platelets from 56 cirrhotic patients and 56 healthy individuals were isolated for in vitro analyses. Autophagy markers (ATG7, BECN1, LC3, and SQSTM1) were quantified using enzyme-linked immunosorbent assay, while autophagosomes were visualized through electron microscopy. Western blotting was used to assess the autophagy-related proteins and the PDGFR/PI3K/Akt/mTOR pathway following treatment with NaHS (an H2S donor), hydroxocobalamin (an H2S scavenger), or AG 1295 (a selective PDGFR-α inhibitor). A carbon tetrachloride-induced cirrhotic BALB/c mouse model was established. Cirrhotic mice with thrombocytopenia were randomly treated with normal saline, NaHS, or hydroxocobalamin for 15 days. Changes in platelet count and aggregation rate were observed every three days.

Cirrhotic patients with thrombocytopenia exhibited significantly decreased platelet autophagy markers and endogenous H2S levels, alongside increased platelet aggregation, compared to healthy controls. In vitro, NaHS treatment of platelets from severe CTP patients elevated LC3-II levels, reduced SQSTM1 levels, and decreased platelet aggregation in a dose-dependent manner. H2S treatment inhibited PDGFR, PI3K, Akt, and mTOR phosphorylation. In vivo, NaHS significantly increased LC3-II and decreased SQSTM1 expressions in platelets of cirrhotic mice, reducing platelet aggregation without affecting the platelet count.

Diminished platelet autophagy potentially contributes to thrombocytopenia in cirrhotic patients. H2S modulates platelet autophagy and functions possibly via the PDGFR-α/PI3K/Akt/mTOR signaling pathway.

Medication non-adherence among youth with chronic health conditions is a healthcare crisis in the United States. Nearly 20% of youth experience a chronic illness, yet most do not comply with their treatment regimen. Various challenges to adherence arise, such as not understanding the purpose of treatment, painful or difficult administration, forgetfulness, and mood disorders such as anxiety. Cognitive behavioral therapy (CBT) is an empirically supported approach to increasing treatment adherence. Modular CBT incorporates psychoeducation, cognitive restructuring, and behavioral experiments to promote better disease management. This article focuses on the application of CBT to four medical conditions characterized by elevated levels of non-adherence: pill-swallowing difficulties, asthma, type 1 diabetes, and inflammatory bowel disease in youth. The review integrates findings on contextual issues (e.g., ethnocultural variations, the impact of the COVID-19 pandemic), research on non-adherence, and CBT outcome studies. Additionally, limitations of the existing literature and training recommendations are provided.

Despite efforts, tumor recurrence is diagnosed in 35–40% of patients with stage III squamous cell lung carcinoma (SCLC) during the first year after treatment. The purpose of the present investigation was to determine the levels of cytokeratin-fragment 19 (CYFRA 21-1) in blood serum, the percentages of lymphocytes containing chemokine receptor 1 (CXCR1, %, lymphocytes), and the percentages of monocytes containing chemokine receptor 2 (CXCR2, %, monocytes), as well as their combined model before and after treatment for the early detection of recurrence.

Forty-eight patients (29 men and 19 women) with newly diagnosed stage III SCLC were examined. Serum levels of CYFRA 21-1, CXCR1, %, lymphocytes, and CXCR2, %, monocytes in peripheral blood were measured before treatment and at three weeks, three months, and six months after treatment using a chemiluminescence immunoassay analyzer and a flow cytometer, respectively.

The levels of all determined indicators, which were elevated before treatment, decreased sharply three weeks after treatment. Subsequently, three months and six months after treatment, the levels steadily increased in patients with diagnosed tumor recurrence. The differences in these indicators in three weeks to three months, three months to six months, and three weeks to six months after treatment, when included in a regression equation, corresponded to the presence of recurrence with accuracies of 83.3%, 91.7%, and 95.8%, respectively.

Determining the combination of CYFRA 21-1 levels, CXCR1, %, lymphocytes, and CXCR2, %, monocytes in the blood of patients with stage III SCLC is important for assessing the probability of recurrence after treatment.

This review discussed experimental mouse models used in the pre-clinical study of liver fibrosis regression, a pivotal process in preventing the progression of metabolic dysfunction-associated steatohepatitis to irreversible liver cirrhosis. These models provide a valuable resource for understanding the cellular and molecular processes underlying fibrosis regression in different contexts. The primary focus of this review is on the most commonly used models with diet- or hepatotoxin-induced fibrosis, but it also touches upon genetic models and mouse models with biliary atresia or parasite-induced fibrosis. In addition to emphasizing in vivo models, we briefly summarized current in vitro approaches designed for studying fibrosis regression and provided an outlook on evolving methodologies that aim to refine and reduce the number of experimental animals needed for these studies. Together, these models contribute significantly to unraveling the underlying mechanisms of liver fibrosis regression and offer insights into potential therapeutic interventions. By presenting a comprehensive overview of these models and highlighting their respective advantages and limitations, this review serves as a roadmap for future research.

Previous studies suggest that taurine supplementation may attenuate atherosclerosis by reducing lipid levels. However, energy drinks containing taurine have been shown to increase blood pressure, a key risk factor for atherosclerosis. Thus, the role of taurine in atherosclerosis remains controversial. This study aimed to investigate the effect of taurine on the development of atherosclerotic plaques.

Plasma taurine levels were measured in 105 patients with varying degrees of coronary heart disease and in 40 healthy individuals using 1,2-13C2-taurine-based ultra-performance liquid chromatography-tandem quadrupole mass spectrometry (UPLC-QQQ-MS/MS). Apolipoprotein E knockout (ApoE−/−) C57BL/6J mice, fed a high-fat diet and subjected to left carotid artery ligation with cannula insertion, received taurine or saline for four consecutive days. Healthy control mice were fed a normal chow diet and underwent a sham operation. Serum taurine levels, lipid indicators, and arterial histology in the individual mice were examined.

Plasma taurine levels were significantly higher in patients with acute myocardial infarction (4.04 ± 0.24 μg/mL) compared to healthy controls (3.52 ± 0.22 μg/mL). Taurine treatment significantly decreased plaque areas in the carotid artery, reduced Masson’s Trichrome staining, and lowered the ratio of anti-α-SMA to anti-CD68 staining in ApoE−/− mice. Additionally, taurine treatment increased the levels of matrix metalloproteinase 2 in the cultured vascular endothelial cells in vitro.

These findings suggest that taurine supplementation may reduce both the size and stability of atherosclerotic plaques. Therefore, dietary taurine supplements should be used with caution.

Since its proposal, the Model for End-Stage Liver Disease (MELD) score has been employed to predict short-term mortality among patients with chronic liver disease and those awaiting liver transplantation, serving as the primary criterion for organ allocation. However, as the demographic and epidemiological characteristics of chronic liver disease and liver transplantation have evolved, a range of MELD-related scores has emerged, including MELD-Na, iMELD, delta MELD, MELD XI, MELD-LA, and pediatric end-stage liver disease, culminating in the recently proposed MELD 3.0, which builds upon MELD-Na. This study aimed to comprehensively review and summarize relevant studies on MELD 3.0 in various scenarios, assessing its effectiveness in organ allocation, post-transplantation outcomes, and mortality prediction for patients with end-stage liver disease. Our preliminary findings indicate superior predictive performance of MELD 3.0, warranting further in-depth investigations to broaden its clinical implications.

Gastric cancer is the third most common cause of cancer-related death globally. The highest incidence is encountered in Asia, followed by Europe which has the second highest incidence worldwide. In Europe, gastric cancer is typically diagnosed at an advanced stage, with an estimated five-year survival rate of 24%, compared to 59% in Japan. This disparity is largely attributed to the significant role of screening in Japan. Given the expected rise in absolute numbers of gastric cancer cases, there has been a demand for gastric cancer screening programmes in high-intermediate risk countries, advocated by the International Agency for Research on Cancer, the Science Advice for Policy by European Academies, the European Commission as part of the Europe Beating Cancer Plan, and the Maastricht VI/Florence consensus guidelines. This review article summarizes the current disparities in screening strategies between countries in the East and West and comments on future developments in population-based screening research in this field. The references for this article were identified through PubMed, the Cochrane Database of Systematic Reviews, and the Cochrane Controlled Register of Trials using the search terms “gastric cancer”, “stomach cancer”, “Helicobacter pylori”, and “screening” over the period from 1995 until March 2024. Overall, this review identifies three potential approaches to screening: primary, secondary, and opportunistic. It highlights the lack of a uniform consensus on the best approach to screening, the disparity in the information available in different populations, and upcoming research to address this disparity.