Explore the vast range of titles available.

Background Solar radiation is primarily composed of ultraviolet radiation (UVR, 200 − 400 nm) and photosynthetically active radiation (PAR, 400 − 700 nm). Ultraviolet-B (UVB) radiation accounts for only a small proportion of sunlight, and it is the primary cause of plant photodamage. The use of chlorofluorocarbons (CFCs) as refrigerants caused serious ozone depletion in the 1980s, and this had led to an increase in UVB. Although CFC emissions have significantly decreased in recent years, UVB radiation still remains at a high intensity. UVB radiation increase is an important factor that influences plant physiological processes. Ulva prolifera , a type of macroalga found in the intertidal zone, is intermittently exposed to UVB. Alternative oxidase (AOX) plays an important role in plants under stresses. This research examines the changes in AOX activity and the relationships among AOX, photosynthesis, and reactive oxygen species (ROS) homeostasis in U. prolifera under changes in UVB and photosynthetically active radiation (PAR). Results UVB was the main component of solar radiation impacting the typical intertidal green macroalgae U. prolifera . AOX was found to be important during the process of photosynthesis optimization of U. prolifera due to a synergistic effect with non-photochemical quenching (NPQ) under UVB radiation. AOX and glycolate oxidase (GO) worked together to achieve NADPH homeostasis to achieve photosynthesis optimization under changes in PAR + UVB. The synergism of AOX with superoxide dismutase (SOD) and catalase (CAT) was important during the process of ROS homeostasis under PAR + UVB. Conclusions AOX plays an important role in the process of photosynthesis optimization and ROS homeostasis in U. prolifera under UVB radiation. This study provides further insights into the response of intertidal macroalgae to solar light changes.

Named for the characteristic basic helix-loop-helix (bHLH) region in their protein structure, bHLH proteins are a widespread transcription factor class in eukaryotes. bHLHs transcriptionally regulate their target genes by binding to specific positions on their promoters and thereby direct a variety of plant developmental and metabolic processes, such as photomorphogenesis, flowering induction, shade avoidance, and secondary metabolite biosynthesis, which are important for promoting plant tolerance or adaptation to adverse environments. In this review, we discuss the vital roles of bHLHs in plant responses to abiotic stresses, such as drought, salinity, cold, and iron deficiency. We suggest directions for future studies into the roles of bHLH genes in plant and discuss their potential applications in crop breeding.

To evaluate the cost-effectiveness of Tislelizumab vs Sorafenib as the first-line treatment of unresectable hepatocellular carcinoma (HCC) from the perspective of the Chinese health service system. A lifetime partitioned survival model (PSM) was developed to cost-effectively analyze Tislelizumab vs Sorafenib as the first-line treatment of unresectable HCC. The clinical and safety data were derived from a recently randomized clinical trial (RATIONALE-301). Utilities were collected from the published literature. Costs were obtained from an open-access database (http://www.yaozh.com) and previous studies. The model cycle was 21 days, according to the RATIONALE-301 study, and the simulation period was patients' lifetime. Long-term direct medical costs and quality-adjusted life-years (QALYs) were determined. The incremental cost-effectiveness ratio (ICER) was used as the evaluation index. one-way sensitivity analysis (OSWA) and probabilistic sensitivity analysis (PSA) were used to analyze the uncertainty of parameters and to adjust and verify the stability of the baseline results. The Tislelizumab group generated a cost of $39,746.34 and brought health benefits to 2.146 QALYs, while the cost and utility of the Sorafenib group were $26750.95 and 1.578 QALYs, respectively. The Tislelizumab group increased QALYs by 0.568, the incremental cost was $12995.39, and the ICER was $22869.64/QALY, lower than the willingness to pay threshold (WTP). OSWA results showed that the utility of progressed disease (PD), cost of Camrelizumab, and cost of Tislelizumab were the main factors affecting the ICER. PSA results showed that, within 1000 times the Monte Carlo simulation, the cost of the Tislelizumab group was lower than three times the per capita gross domestic product (GDP) of China ($37653/QALY). The cost-effectiveness acceptability curves (CEAC) revealed that when WTP was no less than $12251.00, the Tislelizumab group was the dominant scheme, and the economic advantage grew with an increasing WTP. When WTP ≥ $19000.00, the Tislelizumab group became the absolute economic advantage. Under the current economic conditions in China, the Tislelizumab therapeutic scheme is more cost-effective than the Sorafenib therapeutic scheme for treating patients with unresectable HCC.

Background Understanding sex disparities in stroke can identify gaps in clinical care. The objective of this study was to investigate whether sex differences could influence clinical outcomes of patients with acute vertebrobasilar artery occlusion (VBAO) who underwent endovascular therapy (EVT). Methods Patients were selected from the ANGEL-ACT Registry. The primary outcome was favorable functional outcome (90-day modified Rankin Scale [mRS] 0–3). Secondary outcomes included 90-day mRS distribution, excellent outcome (mRS 0–1), functional independence (mRS 0–2), early neurological improvement, recanalization, intracranial hemorrhage, and mortality within 90 days. The above outcomes were compared by two adjustment models, including (1) multivariable logistics analysis adjusting for all baseline and procedural variables with a P  < 0.05; (2) adjusting for the propensity score. Results There were 347 acute VBAO patients treated with EVT included, of whom 72 (20.7%) were women and 275 (79.3%) were men. Women were older (72[63–76] vs. 62[53–69], P  < 0.001) and had a higher rate of atrial fibrillation (31.9% vs. 8.7%, P  < 0.001), lower rates of underlying intracranial atherosclerotic disease (30.6% vs. 51.3%, P  = 0.007), and tandem occlusion (8.3% vs. 21.8%, P  = 0.009) than men. The rate of favorable outcome (mRS 0–3) was similar between women and men (41.7% vs. 51.3%, adjusted odds ratio 1.56, 95%CI: 0.83–2.95, P  = 0.171). There were no sex differences in other clinical outcomes (all P  > 0.05). Conclusions In the ANGEL-ACT registry, the percentage of men with acute VBAO undergoing EVT was approximately fourfold higher than that of women with acute VBAO undergoing EVT. Sex differences did not modify the outcomes of acute VBAO after EVT.

There were limited studies comparing the anterior (AC) and posterior (PC) circulation acute ischemic strokes (AIS). Our study aimed to evaluate distinct features of AC and PC strokes regarding clinical, vascular risk, pathogenesis and outcome factors after endovascular procedures. This multicenter prospective study registered 873 patients with acute large occlusion of anterior circulation stroke (ACS) and posterior circulation stroke (PCS). Patients who underwent endovascular procedures were included in this study. The differences in ACS and PCS regarding baseline characteristics, post-operative intracranial hemorrhage and outcomes were evaluated. A total of 741 patients were included in the data analysis. Intravenous thrombolysis (31.5%), atrial fibrillation (22.7%) and stent thrombectomy (82.4%) were more frequently observed in ACS patients. While higher NIHSS score, hypertension (67.6%) and balloon angioplasty (20.7%) were more prevalent in PCS patients. Symptomatic intracranial hemorrhage was more common in ACS (7.4% vs 2.8%). However, a 3-month follow-up outcomes were better in ACS with higher functional independence and low mortality rate than PCS (46.8% vs 30.3% and 16.4% vs 33.8%, respectively, P < 0.01). In this large prospective study, there were significant differences in the pathogenesis of stroke and treatment procedure between ACS and PCS which influence the clinical outcome. These findings could lead to a tailored clinical procedures and treatment strategies to improve the prognosis in both groups.

Emerging wearable electronics are anticipated to leverage the flexibility and stretchability of organic solar cells (OSCs). However, achieving a balance between power conversion efficiency (PCE) and mechanical robustness remains challenging, as the molecular structural modifications required for enhanced flexibility of photovoltaic materials typically compromise charge transport and extraction. Herein, we design and synthesize three star-branched polymer donors (SPDs: S1, S2, and S3) by introducing different contents of 1,3,5-tris(bromomethyl)benzene, which boost fracture strain compared to the linear PM6 (12.70%, 15.33% and 19.16% to 10.46%), improving devices’ stress resistance/fatigue endurance. More importantly, these SPDs are able to self-assemble into refined fibrous architectures to retain perfect optoelectronic properties: S2:L8-BO OSCs reach 19.51% (rigid), 18.39% (flexible), 15.40% (stretchable); ternary ones hit 20.48%. This molecular engineering strategy successfully overcomes the unfavorable competition between efficiency and mechanical compliance, paving the way for the commercialization of high-performance OSCs as reliable power sources for wearable electronics. Balancing power conversion efficiency and mechanical robustness in flexible electronics remains challenging. Here, the authors introduce 1,3,5-tris(bromomethyl)benzene into polymer donors as a crosslinker to improve the devices’ flexibility while achieving 20.48% efficiency in ternary organic solar cells.

Atherosclerosis is mediated by circulating monocytes and lesional macrophages through chronic inflammation accompanied by metabolic reprogramming. Although methionine metabolism enhances the proinflammatory capacity of monocytes/macrophages, its role in atherosclerosis remains unclear. Here, we use untargeted metabolomics and mass spectrometry to demonstrate that monocyte methionine metabolism is associated with vulnerable plaque (thin-cap fibroatheroma [TCFA]) identified by pancoronary optical coherence tomography. Methionine adenosyltransferase Ⅱ alpha (MAT2A), the key enzyme of methionine metabolism, is highly expressed in atherosclerosis. Further epigenetic profiling of inflammatory and migratory gene promoters reveals MAT2A-mediated enrichment of the transcriptional permissive chromatin mark H3K4me3. Myeloid-specific MAT2A ablation and pharmacological inhibition, or a low-methionine diet, reduce monocyte/macrophage inflammation and migration, thereby attenuating plaque vulnerability. Mechanistically, norepinephrine activates the mTOR-c-MYC axis to upregulate MAT2A expression. The combination of norepinephrine and methionine metabolism is associated with TCFA presence and 5-year clinical prognosis. Consequently, MAT2A-mediated methionine metabolism represents a potential therapeutic target for atherosclerosis. Monocytes/macrophages exert pro-atherogenic functions depending on their metabolic programming. Here, the authors show the pivotal role of methionine metabolism in the proinflammatory and migratory functions of monocytes/macrophages and identify MAT2A as a potential target for the management of atherosclerosis.

Background: In patients with posterior circulation stroke, the association between National Institutes of Health Stroke Scale (NIHSS) scores after thrombectomy and 90-day functional outcomes remains unclear. Objectives: We aimed to explore which factors among the 24-h NIHSS score, ΔNIHSS (baseline NIHSS minus 24-h NIHSS), and NIHSS score change rate (ΔNIHSS/baseline NIHSS × 100%) are associated with favorable functional outcomes at 90 days postoperatively in patients with posterior circulation stroke. Design: We performed a post hoc analysis of a prospective observational study utilizing key techniques of endovascular treatment and emergency workflow improvements from the acute ischemic stroke registry. The study included a cohort of 353 patients who underwent thrombectomy due to posterior circulation stroke. For all patients, we collected baseline characteristics, lesion locations, NIHSS scores, ΔNIHSS (baseline NIHSS minus 24-h NIHSS), NIHSS score change rate (ΔNIHSS/baseline NIHSS × 100), and 90-day postoperative modified Rankin Scale (mRS) score. Methods: A 90-day postoperative mRS score of 0–2 was defined as a favorable functional outcome, while a score of 3–6 was defined as an unfavorable functional outcome. The 24-h NIHSS score and ΔNIHSS score were converted into binary variables based on the Youden index to determine the optimal thresholds that best predict favorable functional outcomes at 90 days postoperatively. Adjusted logistic regression analysis was used to assess the predictive efficacy of the 24-h NIHSS score, ΔNIHSS (baseline NIHSS minus 24-h NIHSS), and NIHSS score change rate (ΔNIHSS/baseline NIHSS × 100) for the 90-day mRS. Subsequently, patients were categorized into cardioembolic embolism (CE) and large artery atherosclerosis (LAA) subgroups according to the Trial of Org 10172 in Acute Stroke Treatment classification, and the predictive efficacy of the optimal thresholds was examined within these subgroups. Results: Multivariate logistic regression analysis revealed that the 24-h NIHSS score was an independent predictor of 90-day functional outcomes (odds ratio (OR): 10.61, 95% confidence interval: 6.44–17.46, p < 0.001). The Youden index identified a 24-h NIHSS score of ⩽9 as the threshold for predicting an mRS score of 0–2, demonstrating good sensitivity (78.5%) and specificity (76.3%). The receiver operating characteristic curve indicated that the predictive model had good discriminative ability (area under the ROC curve = 0.8223). In subgroup analysis, a 24-h NIHSS score of ⩽9 also showed superior predictive efficacy in both the CE (sensitivity 67.8%, specificity 73.5%) and LAA (sensitivity 81.1%, specificity 74.4%) groups. Conclusion: The 24-h postoperative NIHSS score is a reliable predictor of 90-day functional outcomes in patients with posterior circulation stroke undergoing endovascular treatment. The predictive efficacy is optimal when the NIHSS score is ⩽9.

The value of intravascular ultrasound (IVUS) in the diagnosis and treatment of the venous system is not well established. Introducing a novel approach to utilizing IVUS to evaluate cerebral venous sinus (CVS) stenosis and select stent. Idiopathic intracranial hypertension (IIH) patients with CVS stenosis who underwent IVUS-guided stenting were included in the data analysis from January 2014 to February 2022. The degree of maximum stenosis was determined based on the cross-sectional area (CSA) measured by IVUS, and a stent selection method was applied in the study. Follow-up evaluations were conducted at 6 months to 1 year after endovascular treatment to assess symptom improvement. Additionally, repeated digital subtraction angiography (DSA) or Magnetic resonance venography (MRV) / CT venography（CTV） was performed to evaluate the stent patency at 6 months to 1 year post-procedure. The study included 61 patients. IVUS indicated a lower degree of stenosis compared to conventional DSA measurements when evaluating the degree of stenotic segments preprocedure (74.84 ± 10.12% vs. 78.48 ± 8.72%, p  = 0.035). Post-procedural CSA of the most severe stenotic segments showed significant improvement (36.44 ± 8.07 mm 2 vs. 7.42 ± 3.28 mm 2 , p  < 0.001). The stent achieved complete expansion (mean stent expansion index, 0.93 ± 0.20) with no significant change in the structure of the reference segment. The trans-stenotic mean pressure gradients (MPGs) across 61 patients significantly decreased from 11.00 ± 6.23 mmHg to 2.09 ± 2.34 mmHg. 47 out of 61 patients received imaging follow-up; among them, 44 (93.6%) demonstrated stent patency in the follow-up imaging. IVUS has great potential to evaluate the degree and extent of CVS stenosis, assist stent selection, and optimize stent position during the interventional procedure in conjunction with DSA.

Due to the high mortality rate and increasing severity of antibiotic resistance, there is a growing interest in new treatments for ae (KP)-induced pneumonia. Research has shown that the single herbs of SiHuangQingXinWan (SHQXW) are effective in treating pneumonia caused by KP. The PI3K/AKT signaling pathway has garnered attention for its potential role in the management of bacterial infections. This study aimed to evaluate the anti-pneumonia effect of SHQXW and to investigate its mechanism of action. The potential plant metabolites and molecular targets of SHQXW in the context of pneumonia were determined through ultra-high performance liquid chromatography-tandem mass-spectrometry (UHPLC-MS/MS) and bioinformatics analysis. The therapeutic effect of SHQXW was evaluated in a KP-induced pneumonia murine model with imipenem/cilastatin as a positive control. Transcriptomics and non-targeted metabolomics were carried out to unveil potential mechanisms and targets for anti-pneumonia effects. Additionally, an in-depth exploration on the PI3K/AKT signaling pathway was conducted in this study. A total of 24 potential plant metabolites and 285 SHQXW-pneumonia-related targets selected by were identified in this study. The tested doses of SHQXW significantly reduced mortality, improved body weight, decreased the lung index, reduced the bacterial load, and alleviated lung pathological damage in the KP-induced pneumonia murine model ( < 0.05). Notably, 1.3 g/kg/day of SHQXW provided the most effective protective outcome. Furthermore, SHQXW demonstrated the ability to suppress the production of inflammatory factors such as IL-1α, IL-1β, IL-3, IL-6, IL-12p70, G-CSF, GM-CSF, MCP-1, KC, and TNF-α. Analysis of transcriptomic and metabolomic data revealed that SHQXW could modulate inflammation-related signaling pathways (TNF, HIF-1, NF-κB, and PI3K/AKT) and metabolites to regulate pulmonary inflammation. Additional experiments using RT-qPCR and western blotting indicated that SHQXW may exert anti-inflammatory effects by activating the PI3K/AKT pathway. The findings indicate that SHQXW effectively reduces inflammation in mice with KP-induced pneumonia by modulating inflammatory signaling pathways and metabolites, rather than by directly inhibiting the growth of KP. This study introduces a novel treatment approach for KP-induced pneumonia and presents a new outlook on drug development.