Helicobacter pylori (H. pylori) infection can cause multiple secondary digestive disorders. Some studies have found that polymorphisms in Toll-like receptor (TLR) genes, including TLR10 rs10004195, may be associated with increased susceptibility to H. pylori infection. Despite conflicting reports, we conducted a meta-analysis to clarify the relationship between these factors.

We conducted an exhaustive review, encompassing all relevant literature up to February 2024, using databases such as PubMed, Embase, Web of Science, and the China National Knowledge Infrastructure. We screened studies based on specific criteria and evaluated their quality using the Newcastle-Ottawa scale. Heterogeneity testing and meta-analysis were performed using Stata 17.0 software, and SPSSAU was used for publication bias evaluation and sensitivity analysis.

Eight of the 487 identified studies met the inclusion criteria, comprising 3,004 and 2,140 individuals in the H. pylori-positive and negative control groups, respectively. Our results demonstrated that individuals carrying the AA genotype at the TLR10 rs10004195 locus had a significantly increased likelihood of H. pylori infection when analyzed using the recessive genetic model (OR: 1.64, CI: 1.04–2.58, p = 0.034). No statistically significant associations were found in the other four genetic models.

Our findings suggest that carrying the TLR10 rs10004195 AA genotype is associated with a significantly elevated risk of H. pylori infection. This information could be used to assess future risk of H. pylori infection in healthy individuals and provide personalized health guidance based on individual genetic polymorphisms.

The brain, traditionally regarded as immune-privileged due to the blood-brain barrier, harbors a sophisticated immune system crucial for maintaining neural health and resilience against various challenges. Microglia, the resident immune cells of the central nervous system, actively monitor their environment, participating in immune surveillance, synaptic pruning, and neuroprotection. Astrocytes also play vital roles by regulating neurotransmitter levels, supporting metabolism, and maintaining the blood-brain barrier integrity. Recent research underscores the involvement of T cells and monocytes in modulating neuroinflammation and immune responses within the brain. Neurological disorders such as Alzheimer’s and Parkinson’s disease highlight the brain’s vulnerability to immune dysregulation. This review aimed to elucidate the role of neuroimmune cells in brain health and the progression of neurological diseases. It aimed to identify critical mechanisms to enhance therapeutic strategies and improve outcomes. Understanding these interactions is essential for developing targeted therapies to mitigate neuroinflammation and preserve cognitive functions. This review critically examines neuroinflammation related to aging and disease, with a focus on neuroimmune cells and their underlying mechanisms. It highlights how chronic inflammation, driven by activated microglia and astrocytes, exacerbates neuronal damage, synaptic dysfunction, and cognitive decline. The disruption of immune privilege in these conditions involves complex pathways that trigger inflammatory responses, impairing essential neural functions. Despite its immune-privileged status, the brain’s immune system, primarily involving microglia and astrocytes, is crucial for maintaining homeostasis and managing illness. Our review strongly suggests that neurological diseases, influenced by genetic, environmental, and aging factors, often involve heightened neuroinflammation. Targeted therapies are needed to address infections, chronic inflammation, and environmental impacts. Additionally, research into mental health disorders and advancements in imaging techniques are critical for understanding immune dysfunction and enhancing treatment strategies.

Over the course of the COVID-19 pandemic and its aftermath, growing concerns have emerged about the mental health of children and youth. Disease, loss, and lockdowns presented young people with enormous stressors, and much research suggests elevated levels of pediatric depression, anxiety, suicidality, and obsessive-compulsive behavior. However, considerable debate remains about the nature and persistence of these symptoms. This narrative review, conducted approximately four years after the onset of the pandemic, summarizes the major findings from four years of research, including empirical studies, meta-analyses, and systematic reviews. Studies were sourced from scholarly databases using the keywords “COVID-19”, “children”, “adolescents”, and “mental health”. The existing literature on the prevalence of depression in youth indicated that worldwide rates varied from 2.2% to 11.8% of the population, with one study revealing that one in four young people reported depressive symptoms. More specifically, 44% of youth in the United States demonstrated depression, while in China, the prevalence rate ranged from 11% to 44% of young people. Reviewed data showed that 20% of youth globally endorsed symptoms of anxiety or stress reactions, with countries such as Denmark (44%), Canada (45%), and the United States (32%) reporting extremely high rates. In the implications section, recommendations for screening and intervention procedures are outlined.

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.

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.

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.

Tumor hypoxia is a physiologic barrier to radiotherapy and anti-tumor drug delivery. Numerous efforts have been made to overcome this barrier and to improve therapeutic outcomes. Strategies for targeting tumor hypoxia have included chemical radiosensitizers and hyperthermia, followed by combined synergic therapeutic modalities. Clinical hypoxia measurements and the development of molecular imaging agents prompted trials on dose escalation in external beam radiotherapy, which takes advantage of contemporary sophisticated radiation dose delivery techniques. Increases in our understanding of hypoxia-induced biological pathways have led to the investigation of various hypoxia targeting drugs. Radiolabeled hypoxia targeting drugs deliver radionuclides into hypoxic tumor cells and achieve highly localized cell death. In this manuscript, we briefly review the methods of targeting tumor hypoxia in radiotherapy. These include image guided dose escalation in external beam radiotherapy, radiosensitizers, and radiolabeled agents targeting hypoxia pathways and the receptors on hypoxic tumor cells. Our current understanding of tumor hypoxia is the culmination of the collective efforts of generations of researchers. New frontiers are continuing to expand, as new discoveries are being made on both the macroscopic and molecular levels.