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Plants encounter natural antagonist threats of varying intensity and respond by activating multiple defense traits. Due to the fitness costs associated with producing defense traits, plants are expected to activate less costly traits first, reserving more costly defenses for potentially more severe damage (“cheaper first hypothesis”), but evidence to date is scarce. Here, we tested this hypothesis by measuring six putative defense traits in the annual plant Ambrosia artemisiifolia . We found that all traits were effective against insect herbivores, but production of three of them more strongly reduced plant growth, suggesting higher growth costs. When plants were attacked by insect herbivores, less costly traits were induced first, even at the lowest levels of damage, while more costly traits were activated only after higher damage thresholds. This cost-dependent sequential pattern was consistently observed in plants when challenged by 12 different herbivore species from three insect orders. These findings demonstrate that plants can employ the “cheaper first” sequential induction defense strategy, potentially allowing them to reduce defense costs and maximize fitness. Our study provides new insights into how plants fine-tune their defense responses under variable antagonistic pressures.

Colorectal cancer (CRC) is one of the most significant oncological threats to human health globally. Patients often exhibit a high propensity for tumor recurrence and metastasis post-surgery, resulting in suboptimal prognoses. One of the underlying reasons for the metastatic potential of CRC is the sustained abnormal state of the tumor immune microenvironment, particularly characterized by the atypical death of critical immune cells. In recent years, a novel concept of cell death known as PANoptosis has emerged. This form of cell death is regulated by the PANoptosome complex and encompasses key features of apoptosis, pyroptosis, and necroptosis, yet cannot be entirely substituted by any of these processes alone. Due to its widespread occurrence and complex mechanisms, PANoptosis has been increasingly reported in various malignancies, enhancing our understanding of its pathological mechanisms, particularly in the context of CRC. However, the characteristics of immune cell PANoptosis within the CRC immune microenvironment have not been thoroughly elucidated. In this review, we focus on the impact of CRC progression on various immune cell types and summarize the distinctive features of immune cell PANoptosis. Furthermore, we highlight the future research trends and challenges associated with the mechanisms of immune cell PANoptosis in CRC.

Hesperetin (HSP), a natural flavonoid, demonstrates significant therapeutic effects on cardiovascular and cerebrovascular diseases and displays a strong application potential in the aspects of anti-inflammation and anti-oxidation. Cerebral ischemia–reperfusion is accompanied by the generation of inflammatory storms and the accumulation of reactive oxygen species (ROS), ultimately resulting in neuronal damage. While Hesperetin has been widely studied in the treatment of cardiovascular diseases, its potential for treating cerebral ischemia–reperfusion injury remains underexplored. This study aimed to discuss the potential protective mechanism of HSP on cerebral ischemia–reperfusion injury (CIRI). Ferroptosis, a form of cell death driven by iron-dependent phospholipid peroxidation is associated with neuronal damage during cerebral ischemia and subsequent reperfusion injury. Our findings indicate that HSP can confer neuronal protection after CIRI by inhibiting neuronal ferroptosis. Specifically, HSP could significantly up-regulate glutathione (GSH) levels, and up-regulate glutathione peroxidase 4(GPX4) after CIRI, thereby inhibiting cell ferroptosis. Furthermore, we observed a significant reduction in lipid peroxidation products and ROS levels, we have also obtained the same results in vivo animal experiments. In conclusion, HSP played a protective role in CIRI by regulating intracellular iron ions levels, as well as GSH and GPX4 contents to inhibit neuronal ferroptosis after CIRI.

Cutaneous adverse events (CAEs) after treatment with BRAF and MEK inhibitors in patients with melanoma remain incompletely characterized. To determine the association of BRAF and MEK inhibitor treatment with CAEs in patients with melanoma compared with BRAF inhibitor alone. PubMed, Cochrane, Embase and Web of Science were systematically searched for BRAF and MEK inhibitors from database inception through 10 May 2024. Randomized clinical trials reporting on CAEs in patients with melanoma being treated with BRAF and MEK inhibitors compared with patients with melanoma being treated with BRAF inhibitor monotherapy were selected. Pooled Risk ratios (RRs) and 95% CIs were determined using random-effects analyses. The selected end points were alopecia, cutaneous squamous-cell carcinoma, hyperkeratosis, keratoacanthoma, palmoplantar erythrodysaesthesia syndrome, palmoplantar keratoderma, rash, photosensitivity reaction, and skin papilloma. All-grade and high-grade (≥3) CAEs were recorded. Comparing with BRAF and MEK inhibitors, treatment with BRAF inhibitors alone was associated with an increased risk of rash (RR, 0.73; 95% CI, 0.54-0.99; = 0.039; I = 88%), alopecia (RR, 0.28; 95% CI, 0.20-0.41; P < 0.001; I = 76%), hyperkeratosis (RR, 0.30; 95% CI, 0.22-0.41; P < 0.001; I = 56%), palmoplantar erythrodysaesthesia syndrome (RR, 0.21; 95% CI, 0.10-0.47; P < 0.001; I = 81%), palmoplantar keratoderma (RR, 0.39; 95% CI, 0.26-0.57; P < 0.001; I = 29%), Skin papilloma (RR, 0.25; 95% CI, 0.12-0.52; P < 0.001; I = 77%), cutaneous squamous-cell carcinoma (RR, 0.21; 95% CI, 0.11-0.42; P < 0.001; I = 50%), and keratoacanthoma (RR, 0.22; 95% CI, 0.12-0.40; P < 0.001; I = 0%). Therapy with BRAF and MEK inhibitors was associated with a lower risk of CAEs, especially rash, alopecia, hyperkeratosis, palmoplantar erythrodysaesthesia syndrome, palmoplantar keratoderma, skin papilloma, cutaneous squamous-cell carcinoma, and keratoacanthoma, compared with BRAF inhibitor alone. The risks of photosensitivity reaction was similar between the assessed groups. The findings may help to balance between beneficial melanoma treatment and cutaneous morbidity and mortality.

Traumatic brain injuries (TBI) and stroke are major causes of morbidity and mortality in both developing and developed countries. The complex and heterogeneous pathophysiology of TBI and cerebral ischemia‐reperfusion injury (CIRI), in addition to the blood‐brain barrier (BBB) resistance, is a major barrier to the advancement of diagnostics and therapeutics. Clinical data showed that the severity of TBI and stroke is positively correlated with the number of neutrophils in peripheral blood and brain injury sites. Furthermore, neutrophil extracellular traps (NETs) released by neutrophils correlate with worse TBI and stroke outcomes by impairing revascularization and vascular remodeling. Therefore, targeting neutrophils to deliver NETs inhibitors to brain injury sites and reduce the formation of NETs can be an optimal strategy for TBI and stroke therapy. Herein, the study designs and synthesizes a reactive oxygen species (ROS)‐responsive neutrophil‐targeting delivery system loaded with peptidyl arginine deiminase 4 (PAD4) inhibitor, GSK484, to prevent the formation of NETs in brain injury sites, which significantly inhibited neuroinflammation and improved neurological deficits, and improved the survival rate of TBI and CIRI. This strategy may provide a groundwork for the development of targeted theranostics of TBI and stroke. Neutrophils and neutrophil extracellular traps (NETs) play a very important role in TBI and stroke. A neutrophil‐hitchhiking delivery system loaded with PAD4 inhibitor is developed to prevent the formation of NETs in brain injury sites, which significantly inhibits the neuroinflammation, improves the neurological deficits, and prolongs the survival of TBI and stroke.

We demonstrate an all-polarization-maintaining (PM) mode-locked thulium-doped fiber laser operating in the net-normal-dispersion regime based on a figure-9 nonlinear amplifying loop mirror (NALM) configuration. A chirped fiber Bragg grating (CFBG) and a commercial PM dispersion-compensating fiber (PM-DCF) are incorporated into the figure-9 cavity, providing a large normal net dispersion and enabling stable dissipative-soliton mode-locking. Under stable dissipative-soliton operation, the laser delivers a maximum output power of 53.6 mW at a repetition rate of 12.31 MHz, corresponding to a pulse energy of 4.3 nJ. The output spectrum has a central wavelength of ~1952 nm with a 3 dB bandwidth of ~11 nm. The all-PM laser oscillator directly generates a fs pulse without extra-cavity compression, achieving a pulse duration of 545 fs at the CFBG arm. Moreover, stable fundamental mode-locking is verified by a high radio-frequency signal-to-noise ratio (SNR) exceeding 82 dB and a long-term root-mean-square (RMS) power fluctuation of 0.45% over two hours. To the best of our knowledge, this represents the highest output power generated from an all-PM-fiber figure-9 laser oscillator in the 2 μm band, alongside fs-pulse operation. This high-power, compact, stable and environment-insensitive fs-pulsed laser source shows great potential as an ideal seed for biomedical imaging and mid-infrared frequency combs.

1. The shifting defence hypothesis (SDH) predicts that after invasive plants are introduced to new ranges, they will evolve reduced resistance to specialist herbivores and increased resistance to generalist herbivores because they can escape from specialists but are still attacked by generalists in their nonnative ranges. For this to be true, the subsequent introduction of native specialist herbivores should reverse the above evolutionary processes, but evidence collected so far is scarce. 2. Here, we address this research gap by comparing resistance to specialist and generalist herbivores and resistance-related traits in the invasive plant Ambrosia arte misiifolia from five populations with about a decade history of infestation by the accidentally introduced native specialist leaf beetle Ophraella communa (infested populations), and three populations without such infestation history (uninfested populations). 3. In common garden experiments, the specialist O. communa performed better on uninfested populations than on infested populations, whereas two generalist insects, Spodoptera litura and Helicoverpa armigera, performed better on infested populations. Chemical analyses showed that plants from infested populations had lower concentrations of chlorogenic acid, an antigeneralist secondary compound that can attract O. communa. Furthermore, across mother plants from all populations studied, chlorogenic acid content was negatively correlated with larval growth of S. litura and positively correlated with that of O. communa. Finally, quantitative defence traits did not differ between infested and uninfested populations. 4. Although our results are most consistent with rapid evolution caused by enemy reassociation, we cannot exclude the possibility that observed differences in resistance result from multiple introductions or selections from other environmental factors. 5. Synthesis. These results suggest that reassociation with a specialist herbivore from the native range may result in a rapid evolution of increased resistance to specialist herbivores and reduced resistance to generalist herbivores in the introduced range, which is likely to be mediated by the reduced production of secondary chemicals that can deter generalists while attracting the introduced specialist. This study supports the shifting defence hypothesis (SDH) from a new viewpoint, emphasizing the importance of incorporating the impacts of both specialist and generalist herbivores when evaluating the long-term control effects of classical biological control programmes.

A ZSM-5-based catalyst was prepared by spray-dry method for fluidized-bed naphtha catalytic cracking. Multi-techniques, such as X-ray diffraction, scanning electron microscope, 27 Al MAS NMR, and NH 3 –TPD, were employed for the investigation of ZSM-5 framework stability, framework dealumination, and catalyst acidity variation in hydrothermal treatment. Catalytic performances of fluidized-bed naphtha catalytic cracking at 630–680 °C indicated that light olefins and other value-added products could be more efficiently produced compared with the commercial process of thermal steam cracking. Long-term catalytic evaluation implied that naphtha catalytic cracking over the catalyst prepared with spray-dry method and hydrothermal treatment can be carried out at a variable reaction condition with a relatively high and stable light olefins yield.

The coupled reaction of n-hexane and ethanol over HZSM-5 zeolite has been, for the first time, investigated with a pulse-reaction system. The catalytic reaction results showed an improvement of the initial conversion activity of n-hexane when ethanol was introduced as co-reactant. The FT-IR analysis revealed that the ethanol molecules adsorbed on Brønsted acidic sites were immediately transformed into surface ethoxy groups, which were active species for converting n-hexane and improving the initial conversion activity of n-hexane by a bimolecular hydride transfer mode. Also, the catalytic tests suggested that alkenes resulting from the transformation of ethanol could not enhance the initial conversion of n-hexane compared to active ethoxy groups at the shortest contact time. A mechanism involving the ethoxy groups was proposed to understand the coupled reaction of ethanol and n-hexane.

Spinal cord injury (SCI) is a serious clinical condition characterised by extensive mechanical damage that compromises the tissue structure and microenvironment of the affected area. This damage leads to the formation of fibrotic blood vessels and impaired energy metabolism, both of which hinder recovery. Felodipine, a clinically approved antihypertensive drug, acts as a selective calcium antagonist, primarily inhibiting extracellular calcium influx in arteriolar smooth muscle and selectively dilating arterioles. Additionally, felodipine has been demonstrated to induce autophagy. Considering these properties collectively, we hypothesised that felodipine could modulate the microenvironment of the injured spinal cord. In this study, we employed immunofluorescence and Western blot analyses to evaluate the effects of felodipine on microenvironment repair and neuroprotection, both in vitro and in vivo. Particular attention was given to its regulatory role in AMPK‐mTOR pathway‐mediated macrolipophagy. Our results demonstrated that felodipine effectively improved the injured spinal cord microenvironment by activating macrolipophagy, facilitating the clearance of myelin debris. Furthermore, felodipine promoted the restoration of endothelial cell tight junctions, thereby enhancing the integrity of the blood–spinal cord barrier. This attenuation of barrier disruption after SCI contributed to improved neuronal survival. These findings expanded the clinical application prospect of felodipine and presented new therapeutic avenues for treating SCI.