Perioperative anaphylaxis is a rare, life-threatening, iatrogenic condition that predominantly arises following anesthesia. The unique context of this condition, characterized by the concurrent administration of multiple drugs, patient draping, and altered physiological states, presents significant diagnostic and therapeutic challenges, contributing to a higher mortality rate compared to anaphylaxis in other settings. This narrative review synthesizes the evidence to delineate the evolving etiology, pathophysiology, atypical clinical presentation, evidence-based immediate management, and strategic prevention of perioperative anaphylactic reactions. The primary causative agents include neuromuscular blocking agents, antibiotics, and latex, with emerging culprits such as chlorhexidine, dyes, and novel agents like remimazolam. Diagnosis is complicated by the paucity of cutaneous signs; thus, cardiovascular collapse combined with a low end-tidal carbon dioxide level has emerged as a useful supportive diagnostic indicator that requires integration with the clinical context. Immediate management prioritizes the prompt administration of epinephrine and aggressive fluid resuscitation. Subsequent allergological investigations, primarily via skin testing and serum tryptase/histamine measurement, are paramount for identifying the causative agent and preventing its recurrence. Prevention strategies emphasize meticulous history-taking, risk stratification, and the creation of latex-free environments. Future directions must focus on establishing global surveillance networks, exploring novel biomarkers and risk factors such as the circulating microbiome—a preliminary but promising area of research—and enhancing team preparedness through simulation training to improve patient safety outcomes.

Obstructive sleep apnea (OSA) is a prevalent sleep disorder characterized by intermittent hypoxia and sleep fragmentation, which may contribute to lung cancer development and progression. This review synthesizes epidemiological evidence on the association between OSA and lung cancer incidence and mortality, highlighting inconsistencies due to study design, population differences, and confounding factors such as smoking and obesity. While some studies report an increased lung cancer risk, particularly with severe nocturnal hypoxemia, others suggest no significant association or a potential protective effect. Pathophysiologically, OSA promotes oncogenesis through hypoxia-inducible factor activation, tumor immune microenvironment remodeling, exosome-mediated signaling, nuclear factor κB pathway activation, and enhanced cancer stem cell properties. Continuous positive airway pressure therapy may mitigate these effects, with evidence suggesting reduced lung cancer incidence and improved prognosis in adherent patients. This review underscores the need for standardized studies using objective diagnostics and robust confounder adjustment to clarify the OSA–lung cancer link and optimize clinical management.

The incidence and mortality of stroke are gradually increasing. In this context, post-stroke neuronal loss and the related long-term complications, along with costly treatment strategies, are significant concerns for healthcare professionals, and effective, convenient, and inexpensive therapeutic modalities are required. Natural and easily accessible herbal remedies may be the optimal option in post-stroke recovery. This narrative review aims to summarize the neuroprotective properties of Withania somnifera (Ashwagandha) and its therapeutic efficacy in neuronal plasticity and recovery after stroke. Original research articles, reviews, and case studies were sourced from databases such as PubMed, Web of Science, Scopus, Google Scholar, Medline, and Embase. Only full articles published in English up to July 2025 were considered. Keywords including W. somnifera, Ashwagandha, stroke, cerebral ischemia, neurodegeneration, neuronal loss, and post-stroke recovery were utilized for the literature search. It has been found that various plant parts of W. somnifera are abundant in bioactive compounds. The neuroprotective effects of W. somnifera are documented in numerous diseases. Nevertheless, W. somnifera is reported to be involved in modulating various biological pathways to mitigate neuroinflammation, apoptosis, and oxidative stress in stroke. W. somnifera promotes cell proliferation and enhances neurogenesis. Preclinical experiments on murine models show the effectiveness of W. somnifera in post-stroke recovery by enhancing neural plasticity and reducing neuronal loss in the infarct area. Furthermore, W. somnifera boosts neurotransmitter levels, improves motor functions, and enhances memory. It also decreases neutrophil infiltration in the infarct region and lessens neuronal loss. Therefore, the application of W. somnifera may prove advantageous in facilitating post-stroke recovery by enhancing neural function. However, well-designed clinical trials are needed to confirm the efficacy of W. somnifera in post-stroke recovery in humans.

Diabetic nephropathy is the most common microvascular complication of diabetes mellitus. With the increasing prevalence of diabetes mellitus, diabetic neuropathy has become the primary cause of chronic nephropathy cases. Diabetes mellitus and chronic nephropathy exert certain effects on the digestive system. diabetic neuropathy patients also have digestive system symptoms and gastrointestinal diseases, with most presenting such problems as decreased gastrointestinal tract tension, insufficient gastric motility, decreased contractility, and delayed gastric emptying; these problems are often accompanied by symptoms of digestive system dysfunction, such as constipation, dry stool, tenesmus. This article will summarize and discuss the effects and mechanism of diabetic neuropathy involving the digestive system.

The aim of this article was to review the roles of Helicobacter pylori-induced antralization in gastric carcinogenesis and its implications in clinical practice. A search of PubMed/PubMed Central, Web of Science, and China National Knowledge Infrastructure was performed in December 2018 to retrieve all literature related to antralization (or antralisation), pyloric (or pseudopyloric) glands, pyloric (or pseudopyloric) metaplasia, or pyloric (or pseudopyloric) gland metaplasia, and spasmolytic polypeptide-expressing metaplasia (or SPEM). Among the synonyms, antralization and SPEM, which are derived in the same mechanisms at the molecular, cellular and tissue levels, are more commonly used in recent studies. Antralization (or SPEM) is associated with H. pylori infection, atrophic gastritis and intestinal metaplasia, while H. pylori eradication may reverse antralization. It is proposed that H. pylori infection leads to inflammation in the gastric mucosa and apoptosis of the epithelial cells of the proximal stomach, including gastric incisura, body and fundus. The stem cells proliferate and transform into mucous cells and form antral-type mucosa (i.e. antralization). Subsequently, H. pylori-induced antralization, if not controlled, may develop into atrophic gastritis, intestinal metaplasia, dysplasia, and early intestinal-type gastric cancer. Although many biomarkers, including the spasmolytic polypeptide and mucin 6, are specifically expressed in the gastric mucosa with antralization, none of them are evaluated for the clinical diagnosis of antralization. H. pylori-induced antralization (or SPEM) is believed to be an initiating and reversible stage of gastric carcinogenesis. Identification of antralization would help make an early intervention to cease or even reverse the process toward the development of gastric cancer. Currently, the “gold standard” for diagnosing antralization is pathology, which is invasive and time consuming. A non-invasive and convenient method that accurately and specifically diagnoses antralization is urgently required.

This study aimed to examine the difference in expression of matrix metalloproteinases (MMPs) in ameloblastoma and other benign tumors or normal tissue of the jaw, and ameloblastic carcinoma, and to investigate the correlation of expression of MMPs with patient prognosis.

Studies were identified in the major electronic databases (Medline, EMBASE and Cochrane Library) using the keywords “matrix metalloproteinases” and “ameloblastoma” OR “ameloblastic carcinoma”, and a quantitative meta-analysis was conducted.

Fourteen studies were included in this systematic review. Twelve studies representing a total number of 471 cases qualified for the meta-analysis. The analysis revealed a higher MMP-2 expression in ameloblastoma than in the other benign odontogenic tumors, showing a significant inter-group difference (odds ratio [OR]: 5.33; 95% confidence interval (CI): [1.36, 25.62]; p = 0.02). A lower MMP-2 expression was found for the ameloblastoma than in the ameloblastic carcinoma, with a non-significant inter-group difference (OR: 0.12; 95% CI: [0.01, 1.02]; p = 0.05). Finally, a lower MMP-9 expression was found for the follicular subgroup compared to that in other subgroups of ameloblastoma, showing a significant inter-group difference (OR: 0.15; 95% CI: [0.05, 0.48]; p = 0.001).

We found that MMP-2 expression in ameloblastoma is higher than that in other benign tumors or normal tissue of jaw, and that MMP-9 expression in the follicular subgroup of ameloblastoma is lower than that in other pathology subgroups of ameloblastoma. What is more important, the MMPs expression in ameloblastoma was found to be significantly correlated with many clinicopathologic features of ameloblastoma. However, some limitations weakened the power of this meta-analysis.

Curcumin is a polyphenol present in turmeric and is credited with anti-inflammatory, antioxidant, and chemoprotective properties. Questions remain surrounding curcumin’s bioavailability and the mechanism by which it may exert neuroprotective effects. Following PRISMA 2009 guidelines, a systematic review was conducted to identify randomized, placebo-controlled trials investigating the effects of curcumin supplementation on cognitive function in older adults (>50 years). Five databases were searched (CINAHL, Cochrane Library, PubMed, SCOPUS, Web of Science) with five studies identified, each using different forms of curcumin and validated cognitive screening measures, meeting inclusion criteria. Curcumin doses ranged from between 90 and 4,000 mg/day, with significant improvements found in three of the five studies. Firstly, the most recent study found improvements with 90 mg of curcumin twice daily in tests of selective reminding (p = 0.002), visual memory (p = 0.01), and attention (p < 0.0001) over 18 months in non-demented individuals. The second study found improvement in Montreal Cognitive Assessment tool with 1,500 mg/day curcumin over 52 weeks (p = 0.02). Another study found improvement in serial three subtraction task responses after 4 weeks compared with the placebo group (p = 0.044). Of the adverse events reported (n = 58), gastrointestinal symptoms were most common (n = 34). Before curcumin can be recommended to treat or reduce rates of cognitive decline, well-designed trials with standardization in dose, method of assessing cognition, and duration, are required to determine the most bioavailable form of curcumin with minimal adverse effects.

Artificial intelligence (AI) with machine learning tools are used to search, store, and analyze medical data to benefit both physicians and the health of patients in various ways. With the advancement in machine learning algorithms and bioinformatics techniques, AI has become an essential part of modern healthcare society. AI algorithms and deep learning applications support clinicians with managing health records, making diagnoses and clinical decisions, prescribing medication, determining mental health, and imaging analysis. Clinicians gain rapid access to information and research relevant to the needs of the patients. As some algorithms compete with and sometimes outperform clinicians, it is necessary to fully integrate this technology into daily medical practices. However, we must recognize the strengths and weaknesses of AI, and obtain the perspectives of experts outside the medical field to enable the inclusion of the ethical, philosophical, sociological, psychological, behavioral, and economical aspects of machine behavior when understanding the evolving interaction of machines with humans, so that it can be used for advantageous purposes. AI technology cannot be considered a replacement for physicians, rather it can act as multiple task-oriented device support to ease the burden on clinicians so that they can provide better care of life to patients at every level.

Diet is an important modifiable determinant of disease, and it is becoming clear that diet and genetic risk factors are interactive in determining risk for diseases such as cardiovascular disease, diabetes and cancers. Advances in technology have improved our understanding of gene-nutrient interactions, and lead to the development of nutrigenetics, personalized nutrition based on genetics. While evidence is strong for some associations, others remain unclear. As such, the implementation of nutrigenetics remains controversial. While some argue it is not ready for clinical use, it has also been argued that nutrigenetics is unfairly held to a higher standard than traditional nutrition research. Despite the future promise of nutrigenetic testing for improving health outcomes, several barriers in science, technology, acceptance and ethics exist to its implementation. Gene-nutrient associations have been identified in a number of lifestyle-associated diseases, and better understanding of these relationships may lead to improved health outcomes. However, the success of nutrigenetics is not only dependent on the strength of the science, but in consumer acceptance and uptake. This narrative review provides an overview of the current landscape for nutrigenetics in relation to key disease states, and addresses the potential barriers to implementation.