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Background High temperature, whether transitory or constant, causes physiological, biochemical and molecular changes that adversely affect tree growth and productivity by reducing photosynthesis. To elucidate the photosynthetic adaption response and examine the recovery capacity of trees under heat stress, we measured gas exchange, chlorophyll fluorescence, electron transport, water use efficiency, and reactive oxygen-producing enzyme activities in heat-stressed plants. Results We found that photosynthesis could completely recover after less than six hours of high temperature treatment, which might be a turning point in the photosynthetic response to heat stress. Genome-wide gene expression analysis at six hours of heat stress identified 29,896 differentially expressed genes (15,670 up-regulated and 14,226 down-regulated), including multiple classes of transcription factors. These interact with each other and regulate the expression of photosynthesis-related genes in response to heat stress, controlling carbon fixation and changes in stomatal conductance. Heat stress of more than twelve hours caused reduced electron transport, damaged photosystems, activated the glycolate pathway and caused H 2 O 2 production; as a result, photosynthetic capacity did not recover completely. Conclusions This study provides a systematic physiological and global gene expression profile of the poplar photosynthetic response to heat stress and identifies the main limitations and threshold of photosynthesis under heat stress. It will expand our understanding of plant thermostability and provides a robust dataset for future studies.

Rational design and synthesis of superior electrocatalysts for ethanol oxidation is crucial to practical applications of direct ethanol fuel cells. Here, we report that the construction of Pd-Zn dual sites with well exposure and uniformity can significantly improve the efficiency of ethanol electro-oxidation. Through synthetic method control, Pd-Zn dual sites on intermetallic PdZn nanoparticles, Pd-Pd sites on Pd nanoparticles and individual Pd sites are respectively obtained on the same N-doped carbon coated ZnO support. Compared with Pd-Pd sites and individual Pd sites, Pd-Zn dual sites display much higher activity for ethanol electro-oxidation, exceeding that of commercial Pd/C by a factor of ~24. Further computational studies disclose that Pd-Zn dual sites promote the adsorption of ethanol and hydroxide ion to optimize the electro-oxidation pathway with dramatically reduced energy barriers, leading to the superior activity. This work provides valuable clues for developing high-performance ethanol electro-oxidation catalysts for fuel cells. Rational design and synthesis of superior electrocatalysts for ethanol oxidation is crucial to practical applications of direct ethanol fuel cells. Here, authors report the construction of Pd-Zn dual sites with well exposure and uniformity can improve the efficiency of ethanol electro-oxidation.

Fatty acid metabolism has been identified as an emerging hallmark of cancer, which was closely associated with cancer prognosis. Whether fatty acid metabolism-related genes (FMGs) signature play a more crucial role in biological behavior of esophageal squamous cell carcinoma (ESCC) prognosis remains unknown. Thus, we aimed to identify a reliable FMGs signature for assisting treatment decisions and prognosis evaluation of ESCC. In the present study, we conducted consensus clustering analysis on 259 publicly available ESCC samples. The clinical information was downloaded from The Cancer Genome Atlas (TCGA, 80 ESCC samples) and Gene Expression Omnibus (GEO) database (GSE53625, 179 ESCC samples). A consensus clustering arithmetic was used to determine the FMGs molecular subtypes, and survival outcomes and immune features were evaluated among the different subtypes. Kaplan–Meier analysis and the receiver operating characteristic (ROC) was applied to evaluate the reliability of the risk model in training cohort, validation cohort and all cohorts. A nomogram to predict patients’ 1-year, 3-year and 5-year survival rate was also studied. Finally, CCK-8 assay, wound healing assay, and transwell assay were implemented to evaluate the inherent mechanisms of FMGs for tumorigenesis in ESCC. Two subtypes were identified by consensus clustering, of which cluster 2 is preferentially associated with poor prognosis, lower immune cell infiltration. A fatty acid (FA) metabolism-related risk model containing eight genes (FZD10, TACSTD2, MUC4, PDLIM1, PRSS12, BAALC, DNAJA2 and ALOX12B) was established. High-risk group patients displayed worse survival, higher stromal, immune and ESTIMATE scores than in the low-risk group. Moreover, a nomogram revealed good predictive ability of clinical outcomes in ESCC patients. The results of qRT-PCR analysis revealed that the MUC4 and BAALC had high expression level, and FZD10, PDLIM1, TACSTD2, ALOX12B had low expression level in ESCC cells. In vitro, silencing MUC4 remarkably inhibited ESCC cell proliferation, invasion and migration. Our study fills the gap of FMGs signature in predicting the prognosis of ESCC patients. These findings revealed that cluster subtypes and risk model of FMGs had effects on survival prediction, and were expected to be the potential promising targets for ESCC.

Aplastic anemia (AA) is a bone marrow failure syndrome characterized by impaired hematopoiesis and a dysfunctional marrow microenvironment. Bone marrow-derived mesenchymal stem cell (BMSC)-derived exosomes play a crucial role in intercellular communication; however, the role of exosomal anthrax toxin receptor 1 (ANTXR1) in erythroid differentiation remains unclear. Mouse BMSCs were isolated, characterized, and transfected with either ANTXR1-overexpressing or ANTXR1-silencing lentiviral vectors. Exosomes were collected and identified using transmission electron microscopy, nanoparticle tracking analysis, and exosomal marker detection. K562 cells and human cord blood CD34⁺cells were treated with these exosomes. Erythroid differentiation was evaluated through flow cytometry for CD235a and CD71, benzidine staining, RT-qPCR, and Western blot analysis of GATA1 and ALAS2. Apoptosis and inflammatory signaling were examined using flow cytometry, ELISA, Western blotting, and co-immunoprecipitation. TLR4 inhibitor and agonist treatments were applied to verify pathway involvement. BMSC-derived exosomes successfully carried ANTXR1, and their abundance reflected ANTXR1 expression in donor BMSCs. Exosomes enriched in ANTXR1 inhibited erythroid differentiation, as evidenced by reduced CD235a/CD71 expression, decreased GATA1 and ALAS2 levels, and diminished hemoglobin synthesis. In contrast, ANTXR1-deficient exosomes promoted erythroid differentiation and apoptosis while activating the TLR4/MyD88/NF-κB pathway. Pharmacological inhibition of TLR4 attenuated these effects, whereas TLR4 agonist treatment enhanced them. Co-immunoprecipitation further supported an interaction between ANTXR1 and TLR4. BMSC-derived exosomal ANTXR1 suppresses erythroid differentiation, at least in part, by modulating the TLR4/MyD88/NF-κB signaling pathway. These findings identify exosomal ANTXR1 as a potential regulator of erythropoiesis.

This study aims to assess the predictive value of certain markers of inflammation in patients with locally advanced or recurrent/metastatic cervical cancer who are undergoing treatment with anti-programmed death 1 (PD-1) therapy. A total of 105 patients with cervical cancer, who received treatment involving immunocheckpoint inhibitors (ICIs), were included in this retrospective study. We collected information on various peripheral blood indices, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), and prognostic nutritional index (PNI). To determine the appropriate cutoff values for these inflammatory markers, we performed receiver operating characteristic curve (ROC) analysis. Progression-free survival (PFS) was estimated using the Kaplan-Meier method, and we conducted both univariate and multivariate Cox regression analyses to evaluate the prognostic value of these markers. Out of the 105 patients who received ICI treatment, the median progression-free survival (mPFS) was 19.0 months. We obtained the patients’ clinical characteristics, such as age, pathological type, therapy regimen, Figo stage, NLR, PLR, LMR, SII, and PNI from their medical records. The optimal cutoff values for NLR, PLR, LMR, SII, and PNI were determined as 3.76, 218.1, 3.34, 1147.7, 43.75, respectively. In the univariate analysis, age, pathological type, therapy regimen, Figo stage, and LMR were not found to be associated with PFS. However, high NLR( P =0.001), high PLR( P <0.001), high SII( P <0.001), and low PNI ( P =0.003)were all associated with shorter PFS. Multivariate analysis indicated that SII ( P =0.017) was an independent risk factor for PFS. This study highlights the potential use of SII as a predictor of progression-free survival in cervical cancer patients undergoing immunotherapy.

N 6 -methyladenosine (m 6 A) maintains maternal RNA stability in oocytes. One regulator of m 6 A, ALKBH5, reverses m 6 A deposition and is essential in RNA metabolism. However, the specific role of ALKBH5 in oocyte maturation remains elusive. Here, we show that Alkbh5 depletion causes a wide range of defects in oocyte meiosis and results in female infertility. Temporal profiling of the maternal transcriptomes revealed striking RNA accumulation in Alkbh5 −/− oocytes during meiotic maturation. Analysis of m 6 A dynamics demonstrated that ALKBH5-mediated m 6 A demethylation ensures the timely degradation of maternal RNAs, which is severely disrupted following Alkbh5 −/− depletion. A distinct subset of transcripts with persistent m 6 A peaks are recognized by the m 6 A reader IGF2BP2 and thus remain stabilized, resulting in impaired RNA clearance. Additionally, reducing IGF2BP2 in Alkbh5 -depleted oocytes partially rescued these defects. Overall, this work identifies ALKBH5 as a key determinant of oocyte quality and unveil the facilitating role of ALKBH5-mediated m 6 A removal in maternal RNA decay. N6-methyladenosine (m6A) maintains maternal RNA stability in oocytes. Here, the authors identify demethylase ALKBH5 as a key determinant of oocyte quality and unveil the facilitating role of ALKBH5-mediated m6A removal in maternal RNA decay.

Radiation-induced lymphopenia (RIL) is closely related to the prognosis of cervical cancer patients and may affect the efficacy of immune checkpoint inhibitors (ICIs). However, the factors influencing RIL are not very clear. In addition to bone marrow (BM) dose-volume, animal studies indicate radiation-induced bowel injury may be a more crucial factor. Further clarification of the correlation between RIL and bowel dose-volume is important for cervical cancer treatment. Cervical cancer patients treated with postoperative radiotherapy or radical radiotherapy were eligible for this retrospective study. Clinical characteristics, dose parameters of bowel and BM, planning target volume (PTV) size, overall survival (OS) and progression-free survival (PFS) were recorded. The absolute lymphocyte count<0.5×10 /L at radiotherapy end was defined as severe RIL (sRIL). Hazard ratio (HR) and 95% confidence interval (Cl)were estimated using Cox regression models. Survival curve was plotted using the Kaplan-Meier method. On this basis, the receiver operating characteristics (ROC) curve was used to calculate the area under the curve (AUC) for radiation parameters with sRIL as the state variable. A total of 118 cervical cancer patients were included in this study, with a median follow-up time of 57.6 months. In multivariable Cox regression analysis, international Federation of Gynecology and obstetrics (FIGO) stage (HR, 11.806; 95% CI, 3.256-42.809; p<0.001), concurrent chemotherapy (HR, 0.200; 95% CI, 0.054-0.748; p=0.017), sRIL after radiotherapy (HR, 6.009; 95% CI, 1.361-26.539; p=0.018), and pathological type (HR, 2.261; 95% CI, 1.043-4.901; p=0.039) were significantly correlated with OS. Patients with sRIL had significantly decreased OS (79.1% vs 94.1%; HR, 3.81; 95%CI, 1.46-9.92; p=0.023). In binary logistic regression analysis, sRIL was significantly correlated with bowel V45 (Odds radio (OR), 1.025; 95%CI, 1.007-1.044; p=0.007), BM V10 (OR, 0.987; 95%CI, 0.978-0.997; p=0.011), BM V20 (OR, 1.017; 95%CI, 1.002-1.031, p=0.027), and PTV size (OR, 0.998; 95%CI, 0.996-1.000; p=0.026). The ROC curve showed, bowel V45 (AUC=0.787, p<0.001) was the best indicator for predicting sRIL. SRIL after radiotherapy could significantly predict decreased OS. In addition, sRIL is associated with higher bowel, BM dose-volume, PTV size, indicating that the bowel may be an important organ leading to an increased risk of sRIL.

Background To identify the factors influencing pyrotinib-induced severe diarrhea and to establish a risk prediction nomogram model. Methods The clinical data of 226 patients received pyrotinib from two medical institutions from January 2019 to December 2023 were analysed retrospectively. A training set was made up of 167 patients from Hainan Cancer Hospital, and the external validation set was made up of 59 patients from Hainan West Central Hospital. Univariate and multivariate logistic regression analysis were used to identify independent factors influencing pyrotinib-induced severe diarrhea, and a risk prediction nomogram model was constructed, which was verified on patients in the external validation set. Results History of adverse reactions (ADRs), initial dose of pyrotinib, combination with capecitabine, thrombocytopenia, aspartate transaminase (AST), and use of probiotics or other drugs that regulate the gut microbiota were identified as independent influencing factors for pyrotinib-induced severe diarrhea (all P  < 0.05). Based on these, a risk prediction nomogram model of pyrotinib-induced severe diarrhea was established. The area under the receiver operating characteristic curve was 0.794 and 0.863 in the training set and the external validation set, respectively. The calibration curve of the prediction model displayed good consistency both the two sets, which indicated that the model could have favourable predictive ability. Conclusion The risk prediction nomogram model of pyrotinib-induced severe diarrhea constructed in this study may identify high risk populations earlier so that clinicians can make appropriate decisions in time.

Folate is a B-vitamin required for DNA synthesis, methylation, and cellular division, whose deficiencies are associated with various disorders and diseases. Currently, most folic acid used for fortification is synthesized chemically, causing undesirable side effects. However, using folate-producing probiotics is a viable option, which fortify folate in situ and regulate intestinal microbiota. In this study, the folate production potential of newly isolated strains from raw milk was analyzed by microbiological assay. Latilactobacillus sakei LZ217 showed the highest folate production in Folic Acid Assay Broth, 239.70 ± 0.03 ng/μL. The folate produced by LZ217 was identified as 5-methyltetrahydrofolate. LZ217 was tolerant to environmental stresses (temperature, pH, NaCl, and ethanol), and was resistant to gastrointestinal juices. Additionally, the in vitro effects of LZ217 on human gut microbiota were investigated by fecal slurry cultures. 16S rDNA gene sequencing indicated that fermented samples containing LZ217 significantly increased the abundance of phylum Firmicutes and genus Lactobacillus, Faecalibacterium, Ruminococcus 2, Butyricicoccus compared to not containing. Short-chain fatty acids (SCFAs) analysis revealed that LZ217 also increased the production of butyric acid by fermentation. Together, L. sakei LZ217 could be considered as a probiotic candidate to fortify folate and regulate intestinal microecology.

Rapid and safe hemostasis is crucial for the survival of bleeding patients in prehospital care. It is urgent to develop high performance hemostatic material to control the massive hemorrhage in the military field and accidental trauma. In this work, an efficient protein hemostat of thrombin was immobilized onto commercial gauze, which was mediated by self-polymerization and anchoring of tannic acid (TA). Through TA treatment, the efficient immobilization of thrombin was achieved, preserving both the biological activity of thrombin and the physical properties of the dressing, including absorbency, breathability, and mechanical performance. Moreover, in the presence of TA coating and thrombin, Gau@TA/Thr could obviously shortened clotting time and enriched blood components such as plasma proteins, platelets, and red blood cells, thereby exhibiting an enhanced in vitro coagulation effect. In SD rat liver volume defect and artery transection hemorrhage models, Gau@TA/Thr still had outstanding hemostatic performance. Besides, the Gau@TA/Thr gauze had inherent antibacterial property and demonstrated excellent biocompatibility. All results suggested that Gau@TA/Thr would be a potential candidate for treating uncontrollable hemorrhage in prehospital care.