Edible insects have emerged as promising sustainable feed ingredients capable of supporting both animal production and gastrointestinal health. Beyond their nutritional value, insect-derived meals contain bioactive compounds—including chitin, antimicrobial peptides, medium-chain fatty acids, micronutrients, and antioxidant molecules—that may modulate gut microbiota–host interactions in farmed monogastric animal species. This review critically examines current evidence on the mechanisms through which insect-based diets influence gastrointestinal physiology in livestock and aquaculture species. Available studies indicate that dietary insect inclusion can promote beneficial shifts in gut microbial communities, including increased bacterial diversity, enrichment of short-chain fatty acid-producing taxa, and reductions in selected opportunistic pathogens. However, these responses are not uniform across experimental models and depend on factors including insect species, processing method, dietary inclusion level, host species, age, and physiological status. Rather than acting through isolated mechanisms, insect-derived bioactive compounds function as an integrated nutritional matrix that simultaneously influences microbial metabolism, epithelial signaling, and immune regulation. Future standardized and multi-omics studies will be essential to identify the principal bioactive compounds responsible for these physiological effects and to optimize insect-derived functional ingredients for precision animal nutrition and more sustainable livestock and aquaculture production.
Heat stroke, a life-threatening condition characterized by core hyperthermia (≥40 °C), central nervous system dysfunction, and multi-organ failure with mortality rates of 20–70%, is increasingly recognized as a systemic inflammatory and hemodynamic disorder rather than a purely thermoregulatory collapse. Among the emerging mediators of its pathophysiology, trimethylamine N-oxide (TMAO)—a gut microbiota-derived metabolite generated from dietary choline, L-carnitine, and betaine—has attracted growing attention as a molecular link between heat-induced gut dysbiosis and multi-organ injury. This review synthesizes current evidence on the physiological and molecular mechanisms whereby TMAO is proposed to aggravate heat stroke pathology, including: (1) NLRP3 inflammasome activation via ROS-TXNIP, SIRT3-SOD2-mtROS, and cathepsin B-mediated pathways; (2) endothelial dysfunction through tight junction disruption, eNOS/NO suppression, and ALDH2/ROS/GSDMD-dependent pyroptosis; (3) platelet hyperreactivity and thrombosis through enhanced Ca2+ mobilization and IP3 signaling; (4) mitochondrial oxidative stress and bioenergetic failure; and (5) neuroinflammation via the gut–brain axis. We further discuss the concentration-dependent duality of TMAO as a chemical chaperone versus a pathological mediator, and evaluate translational strategies targeting TMAO metabolism, including gut microbiota modulation, TMA lyase inhibition, and NLRP3 blockade. Importantly, the majority of the mechanistic evidence synthesized herein derives from disease models other than heat stroke (e.g., atherosclerosis, chronic kidney disease, obesity, aging, preeclampsia, and ischemic stroke); direct evidence obtained in heat-stroke settings remains limited, and several proposed pathways should be regarded as hypotheses awaiting heat-stroke-specific validation. Elucidating TMAO-dependent mechanisms may therefore inform future biomarker development and therapeutic investigation—both of which require clinical validation in heat-stroke patients—in this increasingly prevalent climate-sensitive disease.
BackgroundVisual field defects associated with brain diseases may arise from stroke, intracranial space-occupying lesions, and other central visual pathway disorders. Patient questions often span symptom recognition, explanation of causes, care triage, treatment, and rehabilitation. Large language models may improve access to patient education. However, their accuracy, logic, coherence, safety, and content accessibility have not been compared under controlled conditions in this high-risk, interdisciplinary Chinese-language setting. This study aimed to compare the performance of five selected large language models across multiple dimensions.MethodsIn this cross-sectional study, 30 fixed Chinese-language questions, refined by experts and phrased from a patient perspective, were submitted to ChatGPT 5.6 Sol, DeepSeek V4 Flash, Gemini 3.7 Flash, Qwen 3.8 Max, and Kimi K3 through a unified application programming interface (API) client. Each model generated one response per question in an independent single-turn session, with web retrieval disabled and conversation history cleared. Three raters, blinded to model identity, independently scored 150 randomly presented responses from 1 to 5 for accuracy, logic, coherence, safety, and content accessibility. Response time, word count, non-space character count, sentence count, paragraph count, and table count were also recorded. Models were compared using the Friedman test followed by Bonferroni-adjusted Wilcoxon signed-rank tests. Inter-rater agreement was assessed using Kendall’s W. Correlations were assessed using Spearman analysis with Benjamini-Hochberg false discovery rate correction.ResultsAgreement among the three raters was high across all five dimensions (Kendall’s W = 0.820–0.844; all P < 0.001). The five models differed in accuracy, coherence, and content accessibility (P < 0.001, P < 0.001, and P = 0.001, respectively). No statistically significant between-model differences were observed in logic or safety (P = 0.247 and P = 0.061, respectively). ChatGPT 5.6 Sol had the highest median accuracy score [4.67 (interquartile range, 4.00–5.00)], and Kimi K3 had the highest median coherence score [4.50 (4.00–5.00)]. Both models had a median content accessibility score of 4.67 (4.00–5.00). Response time, response length, and text structure also differed among models. However, their correlations with expert quality scores were generally weak (|ρ| ≤ 0.279).ConclusionThe five large language models exhibited distinctly multidimensional performance when answering Chinese-language patient questions about visual field defects associated with brain diseases. No single model consistently performed best across all clinically relevant dimensions. These findings are specific to the model versions tested on 15 August 2026; stability across repeated generations was not assessed. Response speed, length, and structure cannot substitute for direct assessment of medical quality. The absence of a statistically significant difference in safety ratings under controlled conditions does not imply equivalent or adequate clinical safety. Large language models are better suited to supporting patient education and clinician-patient communication under clinical supervision than to making diagnostic or treatment decisions independently.
BackgroundOcean acidification (OA) represents a growing threat to marine biodiversity, particularly affecting the sensitive early life stages of invertebrates. While the physiological impacts of OA are widely recognized, its specific effects on organogenesis and the molecular regulation of defensive traits in cephalopods remain poorly understood. This study investigated the influence of acidified seawater on the embryonic development and ink sac formation in the Pharaoh cuttlefish (Sepia pharaonis).MethodsEmbryos were reared under four pH conditions (8.0, 7.7, 7.3, and 6.5). Embryonic growth, survival, hatching success, and ink sac morphogenesis were monitored throughout development. The expression of melanin synthesis–related genes, including tyr, per, and spNOS, was quantified using qRT-PCR.ResultsOcean acidification impaired embryonic development in a pH-dependent manner. Severe acidification (pH 6.5) resulted in complete mortality and no surviving embryos by Day 9, while moderate acidification (pH 7.3) led to delayed development and failure to hatch by Day 11, compared to the hatching observed in the control group. Ink sac development was markedly inhibited under acidified conditions, resulting in reduced size and pigmentation. Consistent with these morphological abnormalities, the expression of melanin synthesis markers, including tyrosinase (tyr) and peroxidase (per), exhibited a biphasic response, with early transient induction followed by consistent downregulation across all acidified treatments, while, the expression of the regulatory gene Sepia pharaonis nitric oxide synthase (spNOS) was significantly suppressed under severe acidification.ConclusionsThese findings provide evidence that OA is associated with disrupted embryogenesis and impaired ink sac formation in S. pharaonis, accompanied by altered expression of melanin synthesis-related genes. The resulting reduction in defensive capacity may increase the vulnerability of hatchlings and potentially affect population recruitment under future ocean acidification scenarios.
Pollination by honeybees is vital for maintaining the health of both ecological and agricultural systems. However, honeybee health is often influenced by multiple environmental stresses. Therefore, identifying the key genes involved in stress responses and investigating the molecular mechanisms through which honeybees respond to environmental stress are crucial. In this study, we report that Apis cerana cerana DnaJC28 (AccDnaJC28) is a typical DnaJ protein belonging to the heat shock protein subfamily that contains a J domain and is localized in the cytoplasm. The mRNA levels of AccDnaJC28 were higher in the thorax than in other tissues and in 1-day-old workers than in bees at other developmental stages. Several environmental stressors induced the expression of AccDnaJC28. Functional analyses revealed that silencing AccDnaJC28 decreased the thermotolerance of A. cerana cerana, whereas its overexpression increased the survival of Drosophila S2 cells under heat stress. These results indicate the crucial role of AccDnaJC28 in the stress response and its potential suitability as a novel biomarker. Mechanistic analysis further revealed that knockdown of AccDnaJC28 reduced both the enzymatic activity of certain antioxidant enzymes and the expression levels of related antioxidant genes. In addition, the upregulated expression of certain antioxidant genes may partially compensate for the functional deficiency caused by AccDnaJC28 knockdown. Taken together, our findings demonstrate that AccDnaJC28 is essential for the response of A. cerana cerana to environmental stress, as it mitigates oxidative damage via the antioxidant signaling pathway. These results contribute to the understanding of the foundational defense mechanisms initiated by honeybees in response to environmental stress.
