Longitudinal change of serum AIM2 levels after aneurysmal subarachnoid hemorrhage and its prognostic significance: a two-center prospective cohort study.

Absent in melanoma 2 (AIM2) is implicated in neuroinflammation. Here, we explored the prognostic significance of serum AIM2 in human aneurysmal subarachnoid hemorrhage (aSAH). We conducted a consecutive enrollment of 127 patients, 56 of whom agreed with blood-drawings not only at admission but also at days 1, 2, 3, 5, 7 and 10 days after aSAH. Serum AIM2 levels of patients and 56 healthy controls were measured. Disease severity was assessed using the modified Fisher scale (mFisher) and World Federation of Neurological Surgeons Scale (WFNS). Neurological outcome at poststroke 90 days was evaluated via the modified Rankin Scale (mRS). Univariate analysis and multivariate analysis were sequentially done to ascertain relationship between serum AIM2 levels, severity, delayed cerebral ischemia (DCI) and 90-day poor prognosis (mRS scores of 3-6). Patients, in comparison to controls, had a significant elevation of serum AIM2 levels at admission and at days 1, 2, 3, 5, 7 and 10 days after aSAH, with the highest levels at days 1, 2, 3 and 5. AIM2 levels were independently correlated with WFNS scores and mFisher scores. Significantly higher serum AIM2 levels were detected in patients with a poor prognosis than in those with a good prognosis, as well as in patients with DCI than in those without DCI. Moreover, serum AIM2 levels independently predicted a poor prognosis and DCI, and were linearly correlated with their risks. Using subgroup analysis, there were no significant interactions between serum AIM2 levels and age, gender, hypertension and so on. There were substantially high predictive abilities of serum AIM2 for poor prognosis and DCI under the receiver operating characteristic curve. The combination models of DCI and poor prognosis, in which serum AIM2, WFNS scores and mFisher scores were incorporated, showed higher discriminatory efficiencies than anyone of the preceding three variables. Moreover, the models are delineated using the nomogram, and performed well under the calibration curve and decision curve. Serum AIM2 levels, with a substantial enhancement during early phase after aSAH, are closely related to bleeding severity, poor 90-day prognosis and DCI of patients, substantializing serum AIM2 as a potential prognostic biomarker of aSAH.

Tumor treating fields in glioblastoma: long-term treatment and high compliance as favorable prognostic factors.

Introduction: Tumor treating fields (TTFields) have earned substantial attention in recent years as a novel therapeutic approach with the potential to improve the prognosis of glioblastoma (GBM) patients. However, the impact of TTFields remains a subject of ongoing debate. This study aimed to offer real-world evidence on TTFields therapy for GBM, and to investigate the clinical determinants affecting its efficacy. Methods: We have reported a retrospective analysis of 81 newly diagnosed Chinese GBM patients who received TTFields/Stupp treatment in the Second Affiliated Hospital of Zhejiang University. Overall survival (OS) and progression-free survival (PFS) were analyzed using Kaplan-Meier method. Cox regression models with time-dependent covariates were utilized to address non-proportional hazards and to assess the influence of clinical variables on PFS and OS. Results: The median PFS and OS following TTFields/STUPP treatment was 12.6 months (95% CI 11.0-14.1) and 21.3 months (95% CI 10.0-32.6) respectively. Long-term TTFields treatment (>2 months) exhibits significant improvements in PFS and OS compared to the short-term treatment group (≤2 months). Time-dependent covariate COX analysis revealed that longer TTFields treatment was correlated with enhanced PFS and OS for up to 12 and 13 months, respectively. Higher compliance to TTFields (≥ 0.8) significantly reduced the death risk (HR=0.297, 95%CI 0.108-0.819). Complete surgical resection and MGMT promoter methylation were associated with significantly lower risk of progression (HR=0.337, 95% CI 0.176-0.643; HR=0.156, 95% CI 0.065-0.378) and death (HR=0.276, 95% CI 0.105-0.727; HR=0.249, 95% CI 0.087-0.710). Conclusion: The TTFields/Stupp treatment may prolong median OS and PFS in GBM patients, with long-term TTFields treatment, higher TTFields compliance, complete surgical resection, and MGMT promoter methylation significantly improving prognosis.

Investigation of the pan-cancer property of FNDC1 and its molecular mechanism to promote lung adenocarcinoma metastasis.

BACKGROUND: Fibronectin type III domain containing 1 (FNDC1) has been associated with the metastasis of many tumors, but its function in lung cancer remains uncertain. METHODS: FNDC1 expression was analyzed in The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx), evaluate its prognostic value. Gene Set Enrichment Analysis (GSEA) enrichment analysis of differential expression of FNDC1 in lung cancer. The expression of FNDC1 was detected in five types of lung cancer cells, and screened to establish FNDC1 stable knockdown cell strains. To observe the migration and invasion ability of lung cancer cells after FNDC1 knockdown. Finally, we used rhIL-6 to interfere with the stable knockdown of FNDC1 in A549 cells and observed the recovery of migration and invasion. RESULT: Our results showed that FNDC1 expression was increased in 21 tumor tissues, including lung cancer, and was associated with poor prognosis in five cancers, including lung adenocarcinoma (LUAD) (P < 0.05). GSEA enrichment analysis showed that FNDC1 was related to the pathways involved the JAK-STAT signaling pathway. Stable knockdown of FNDC1 in A549 and H292 cells resulted in decreased migration and invasion ability of both cells, accompanied by decreased expression of MMP-2 and Snail, and a significant decline in the expression of p-JAK2 and p-STAT3. The suppressive effect of FNDC1 knockdown on lung cancer cell metastasis counteracted by the JAK-STAT agonist rhIL-6 were presented in the nude mouse metastatic tumor model. CONCLUSION: FNDC1 is implicated in poor prognosis of a diverse range of malignant tumors, which can promote metastasis and invasion of lung cancer through the JAK2-STAT3 signaling pathway.

The Primary Afferents of Trigeminal Autonomic Reflex May not be Nociceptive: A Case Report.

Autonomic symptoms have been long noticed coming along with pain in the head, e.g. Trigeminal Neuralgia, trigeminal autonomic cephalalgias. The symptoms show up during pain attacks, so they are assumed to be activated by the nociceptive afferents of the trigeminal nerve. Here, we present a case with hypersalivation as the complication after percutaneous balloon compression for trigeminal neuralgia, although the patient was pain-free after the treatment. A 71-year-old female with excessive salivation on the affected side after percutaneous balloon compression is described. The patient underwent microvascular decompression several years ago, and both the microvascular decompression and the preoperative imaging examination confirmed that there was no offending vessel at the root entry zone of the trigeminal nerve. After the percutaneous balloon compression, the patient was free of pain, but the autonomic symptoms (hypersalivation) still showed up. The autonomic symptoms which usually came along with pain presented solely as post-percutaneous balloon compression complication in the case. Contrary to popular belief, for the patient who was pain-free after percutaneous balloon compression, the transiently overactivated nerve fibers that led to hypersalivation were not nociceptive afferents of the trigeminal nerve.

Corrigendum: Clinical value of serum complement component 1q levels in the prognostic analysis of aneurysmal subarachnoid hemorrhage: a prospective cohort study.

[This corrects the article DOI: 10.3389/fneur.2024.1341731.].

Simple and Safe Synthesis of Yolk-Shell-Structured Silicon/Carbon Composites with Enhanced Electrochemical Properties.

With its substantial theoretical capacity, silicon (Si) is a prospective anode material for high-energy-density lithium-ion batteries (LIBs). However, the challenges of a substantial volume expansion and inferior conductivity in Si-based anodes restrict the electrochemical stability. To address this, a yolk-shell-structured Si-carbon composite, featuring adjustable void sizes, was synthesized using tin (Sn) as a template. A uniform coating of tin oxide (SnO2) on the surface of nano-Si particles was achieved through a simple annealing process. This approach enables the removal of the template with concentrated hydrochloric acid (HCl) instead of hydrofluoric acid (HF), thereby reducing toxicity and corrosiveness. The conductivity of Si@void@Carbon (Si@void@C) was further enhanced by using a high-conductivity carbon layer derived from pitch. By incorporating an internal void, this yolk-shell structure effectively enhanced the low Li+/electron conductivity and accommodated the large volume change of Si. Si@void@C demonstrated an excellent electrochemical performance, retaining a discharge capacity of 735.3 mAh g-1 after 100 cycles at 1.0 A g-1. Even at a high current density of 2.0 A g-1, Si@void@C still maintained a discharge capacity of 1238.5 mAh g-1.

Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition.

Spontaneous subarachnoid hemorrhage (SAH) is a kind of hemorrhagic stroke which causes neurological deficits in survivors. Huperzine A has a neuroprotective effect, but its role in SAH is unclear. Therefore, we explore the effect of Huperzine A on neurological deficits induced by SAH and the related mechanism. In this study, Evans blue assay, TUNEL staining, immunofluorescence, western blot analysis, and ELISA are conducted. We find that Huperzine A can improve neurological deficits and inhibit the apoptosis of nerve cells in SAH rats. Huperzine A treatment can improve the upregulation of brain water content, damage of blood-brain barrier, fibrinogen and matrix metalloprotein 9 expressions and the downregulation of ZO-1 and occludin expressions induced by SAH. Huperzine A inhibit the expressions of proteins involved in pyroptosis in endothelial cells in SAH rats. The increase in MDA content and decrease in SOD activity in SAH rats can be partly reversed by Huperzine A. The ROS inducer H 2O 2 can induce pyroptosis and inhibit the expressions of ZO-1 and occludin in endothelial cells, which can be blocked by Huperzine A. In addition, the increase in the entry of p65 into the nucleus in endothelial cells can be partly reversed by Huperzine A. Huperzine A may delay the damage of blood-brain barrier in SAH rats by inhibiting oxidative stress-mediated pyroptosis and tight junction protein expression downregulation through the NF-κB pathway. Overall, Huperzine A may have clinical value for treating SAH.

Clinical value of serum complement component 1q levels in the prognostic analysis of aneurysmal subarachnoid hemorrhage: a prospective cohort study.

Objective: To analyze the relationship between serum complement component 1q (C1q) levels and functional prognosis in patients with aneurysmal subarachnoid hemorrhage (aSAH), and to reveal its clinical value. Methods: In this prospective cohort study, we collected clinical data of aSAH patients admitted to the Department of Neurosurgery, Hangzhou First People's Hospital from January 2020 to October 2022. Parameters such as serum C1q levels, Hunt-Hess grade, modified Fisher grade, and the modified Rankin scale (mRS) at 3 months were included for evaluation. Patients were grouped based on the occurrence of delayed cerebral ischemia (DCI). Spearman rank correlation test and Kruskal-Wallis rank sum test were used to analyze the correlation between serum C1q levels, disease severity, and prognosis. Potential risk factors affecting prognosis and the occurrence of DCI were screened through Independent sample t-test or Mann-Whitney U test. Variables with significant differences (p < 0.05) were incorporated into a logistic regression model to identify independent risk factors affecting prognosis and DCI occurrence. Serum C1q levels were plotted as a ROC curve for predicting prognosis and DCI, and the area under the curve was calculated. Results: A total of 107 aSAH patients were analyzed. Serum C1q levels positively correlated with Hunt-Hess grade, modified Fisher grade and mRS (all p < 0.001). Significant differences were observed in C1q levels among different Hunt-Hess grade, mFisher grade and mRS (all p < 0.001). Notably, higher serum C1q levels were seen in the poor prognosis group and DCI group, and correlated with worse prognosis (OR = 36.927, 95%CI 2.003-680.711, p = 0.015), and an increased risk for DCI (OR = 17.334, 95%CI 1.161-258.859, p = 0.039). ROC analysis revealed the significant discriminative power of serum C1q levels for poor prognosis (AUC 0.781; 95%CI 0.673-0.888; p < 0.001) and DCI occurrence (AUC 0.763; 95%CI 0.637-0.888; p < 0.001). Higher C1q levels independently predicted a poor prognosis and DCI with equivalent predictive abilities to Hunt-Hess grade and modified Fisher grade (both p < 0.05). Conclusion: High levels of C1q in the blood is an independent risk factor for poor prognosis and the development of DCI in patients with aSAH. This can more objectively and accurately predict functional outcomes and the incidence of DCI. C1q may have a significant role in the mechanism behind DCI after aSAH.

Long-term survival of stage Ib lung adenocarcinoma with postoperative brain oligometastasis: a case report and literature review.

Lung adenocarcinoma remains one of the most frequent and deadly tumour entities. Early-stage lung adenocarcinoma is extremely difficult to detect and is also easy to recur or metastasize after treatment. Since the new adenocarcinoma classification was presented in 2011, several studies have shown that patients with solid and/or micropapillary (S/MP) predominant patterns showed a worse prognosis. Here we report the case of a 54-year-old woman who was diagnosed with stage Ib lung adenocarcinoma with S/MP components and developed an isolated brain oligometastasis after resection and adjuvant therapy. A craniocerebral operation was performed, combined with radiotherapy and targeted therapy, and the patient eventually achieved a good quality of life. Our work reviews the clinical features of lung cancer complicated with S/MP components, the relationship between MP and epidermal growth factor receptor (EGFR) mutation, as well as treatment strategies for such a patient with postoperative brain oligometastasis of lung adenocarcinoma complicated with EGFR Exon19del mutation.

Fast detection of hypobromous acid in cells and the water environment using a lysosome-targeted fluorescent probe.

A new fluorescent probe SWJT-23 with lysosomal targeting ability for detection of hypobromous acid (HBrO) was synthesised based on the naphthalimide skeleton. This probe exhibited a fast response (within 3s), a low detection limit (1.24 nM), excellent selectivity and a high fluorescence quantum yield (Φ = 0.490). Moreover, SWJT-23 not only realized the sensitive detection of HBrO in cells and water samples, but also was fabricated as a paper-based sensor. In consequence, SWJT-23 is expected to be an efficient and powerful tool for monitoring HBrO in organisms and the environment in realistic scenarios.

Involvement of aquaporin 5 and Na-K-2Cl cotransporter 1 in the pathogenesis of primary focal hyperhidrosis: evidence from the primary sweat gland cell culture.

People with primary focal hyperhidrosis (PFH) usually have an overactive sympathetic nervous system, which can activate the sweat glands through the chemical messenger of acetylcholine. The role of aquaporin 5 (AQP5) and Na-K-2Cl cotransporter 1 (NKCC1) in PFH is still unknown. The relative mRNA and protein levels of AQP5 and NKCC1 in the sweat gland tissues of three subtypes of patients with PFH (primary palmar hyperhidrosis, PPH; primary axillary hyperhidrosis, PAH; and primary craniofacial hyperhidrosis, PCH) were detected with real-time PCR (qPCR) and Western blot. Primary sweat gland cells from healthy controls (NPFH-SG) were incubated with different concentrations of acetylcholine, and the relative mRNA and protein expression of AQP5 and NKCC1 were also detected. NPFH-SG cells were also transfected with si-AQP5 or shNKCC1, and acetylcholine stimulation-induced calcium transients were assayed with Fluo-3 AM calcium assay. Upregulated AQP5 and NKCC1 expression were observed in sweat gland tissues, and AQP5 demonstrated a positive Pearson correlation with NKCC1 in patients with PPH (r = 0.66, P < 0.001), patients with PAH (r = 0.71, P < 0.001), and patients with PCH (r = 0.62, P < 0.001). Upregulated AQP5 and NKCC1 expression were also detected in primary sweat gland cells derived from three subtypes of patients with PFH when compared with primary sweat gland cells derived from healthy control. Acetylcholine stimulation could induce the upregulated AQP5 and NKCC1 expression in NPFH-SG cells, and AQP5 or NKCC1 inhibitions attenuated the calcium transients induced by acetylcholine stimulation in NPFH-SG cells. The dependence of ACh-stimulated calcium transients on AQP5 and NKCC1 expression may be involved in the development of PFH.NEW & NOTEWORTHY The dependence of ACh-stimulated calcium transients on AQP5 and Na-K-2Cl cotransporter 1 (NKCC1) expression may be involved in the development of primary focal hyperhidrosis (PFH).

Altered brain function in classical trigeminal neuralgia patients: ALFF, ReHo, and DC static- and dynamic-frequency study.

The present study aimed to clarify the brain function of classical trigeminal neuralgia (CTN) by analyzing 77 CTN patients and age- and gender-matched 73 healthy controls (HCs) based on three frequency bands of the static and dynamic amplitude of low-frequency fluctuation, regional homogeneity, and degree centrality (sALFF, sReHo, sDC, dALFF, dReHo, and dDC). Compared to HCs, the number of altered brain regions was different in three frequency bands, and the classical frequency band was most followed by slow-4 in CTN patients. Cerrelellum_8_L (sReHo), Cerrelellum_8_R (sDC), Calcarine_R (sDC), and Caudate_R (sDC) were found only in classical frequency band, while Precuneus_L (sALFF) and Frontal_Inf_Tri_L (sReHo) were found only in slow-4 frequency band. Except for the above six brain regions, the others overlapped in the classical and slow-4 frequency bands. CTN seriously affects the mental health of patients, and some different brain regions are correlated with clinical parameters. The static and dynamic indicators of brain function were complementary in CTN patients, and the changing brain regions showed frequency specificity. Compared to slow-5 frequency band, slow-4 is more consistent with the classical frequency band, which could be valuable in exploring the pathophysiology of CTN.

Temporal change of serum xanthine oxidase levels and its relation to clinical outcome of severe traumatic brain injury: a prospective cohort study.

Xanthine oxidase (XO) may be involved in the induction of oxidative stress and inflammation. We measured serum XO levels at multiple days to determine whether it is associated with the severity and prognosis of severe traumatic brain injury (sTBI). In this prospective cohort study, we quantified serum XO levels in 112 sTBI patients and 112 controls. Serum XO levels of patients were measured at admission and at days 1, 3, 5, 7, and 10 after sTBI. Extended Glasgow outcome scale scores of 1-4 at post-trauma 180 days were defined as a poor prognosis. Multivariate analysis was employed to determine the relationship between poor prognosis and serum XO levels at multiple days. Serum XO levels were significantly increased at admission among patients, afterwards elevated gradually, peaked at day 3, and then diminished gradually until day 10, and were substantially higher during 10 days in patients than in controls. Serum XO levels at 6 different days were all correlated with admission Rotterdam computed tomography (CT) scores and Glasgow coma scale (GCS) scores. Serum XO levels at 6 different days were all substantially higher in patients with poor prognosis than in those with good prognosis. Serum XO levels at days 7 and 10, but not at days 1, 3, and 5, had significantly lower area under receiver operating characteristic (AUC) than those at admission. Serum XO levels at admission and at days 1 and 3, but not at day 5, were independently associated with 180-day poor prognosis. Prognostic prediction model containing GCS scores, Rotterdam CT scores, and serum XO levels at admission (or at days 1 and 3) showed substantially higher AUC than GCS scores and Rotterdam CT scores alone. The models were visually described using nomograms, which were comparatively stable under calibration curve and were relatively of clinical benefit under decision curve. Elevated serum XO levels during early period of sTBI are more closely associated with trauma severity and clinical adverse outcomes, assuming that serum XO may serve as a potential prognostic biomarker in sTBI.

A prospective cohort study on serum A20 as a prognostic biomarker of aneurysmal subarachnoid hemorrhage.

BACKGROUND: A20 may be a neuroprotective factor. Herein, we aimed to investigate whether serum A20 levels were associated with disease severity, delayed cerebral ischemia (DCI), and outcome after aneurysmal subarachnoid hemorrhage (aSAH). METHODS: In this prospective cohort study containing 112 aSAH patients and 112 controls, serum A20 levels were quantified. At 90 d poststroke, Modified Rankin Scale (MRS) scores ≥3 were defined as a poor outcome. All correlations and associations were assessed using multivariate analysis. RESULTS: Compared with controls, there was a significant elevation of serum A20 levels in patients (median 123.7 pg/mL vs. 25.8 pg/mL; P<0.001). Serum A20 levels were independently correlated with Hunt-Hess scores (ß 9.854; 95% confidence interval [95% CI] 2.481-17.227, P=0.009) and modified Fisher scores (ß 10.349, 95% CI 1.273-19.424, P=0.026). Independent associations were found between serum A20 levels and poor outcome (odds ratio [OR] 1.015, 95% CI 1.000-1.031, P=0.047) and DCI (OR 1.018, 95% CI 1.001-1.035, P=0.042). Areas under the curve for predicting poor outcome and DCI were 0.771 (95% CI 0.682-0.845) and 0.777 (95% CI 0.688-0.850), respectively. Serum A20 levels ≥128.15 pg/mL predicted poor outcome, with a sensitivity of 73.9% and specificity of 74.2%, and A20 levels ≥160.55 pg/mL distinguished the risk of DCI with 65.5% sensitivity and 89.2% specificity. Its ability to predict poor outcome and DCI was similar to those of Hunt-Hess scores and modified Fisher scores (both P>0.05). CONCLUSION: Enhanced serum A20 levels are significantly associated with stroke severity and poor clinical outcome after aSAH, implying that serum A20 may be a potential prognostic biomarker for aSAH.

Metal organic framework-derived transition metal-doped CoSx nanocage for enhanced visible light-assisted methanol electrocatalytic oxidation.

Designing noble metal-free anode catalysts for visible light-assisted direct methanol fuel cells still remains a significant challenge. In this study, combining the photocatalytic and electrocatalytic properties of CoSx, a visible light-assisted methanol electrocatalytic oxidation strategy was provided. Doping engineering was employed to adjust the electronic structure of CoSx and improve their photoassisted methanol electrocatalytic oxidation activity. Using ZIF-67 as precursor, transition metal-doped CoSx (M-CoSx, M = Zn, Cu, Ni, and Cd) nanocage was synthesized by cation exchange and L-cysteine-controlled etching. Cd doping not only widens the light adsorption to the visible region but also enhances the separation efficiency of photogenerated electron-hole pairs. The electrochemical and photochemical results indicated that the strong oxidative photogenerated hole, OH˙, and O2˙- are beneficial for methanol electrocatalytic oxidation. The synergistic electrocatalytic and photocatalytic effect will be a practical strategy for improving the methanol electrocatalytic oxidation activity of noble metal-free semiconductor catalysts.

Integrating Network Pharmacology and Experimental Validation to Explore the Effects and Mechanisms of Qinghao Biejia Decoction and Its Active Compound Artemisinin B Against Non-Small-Cell Lung Cancer.

Purpose: To explore the pharmacological effects and mechanisms of Qinghao Biejia decoction (QBD) against non-small-cell lung cancer (NSCLC) based on network pharmacology and to verify the anticancer effect of artemisinin B (ART B), the active ingredient of QBD, on H1299 cells. Methods: Ultra-performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (UPLC-QTOF-MS/MS) was applied to explore the chemoprofile of QBD. A zebrafish xenograft model was used to determine the anti-cancer efficacy of QBD. Cell counting kit-8 assay, terminal deoxyribonucleotide transferase-mediated-dUTP nick-end labeling assay; immunofluorescence, and flow cytometry were used to evaluate the in vitro anti-proliferative and pro-apoptotic effects of QBD and ART B on H1299 cells. Subsequently, the related targets and action mechanisms of both QBD and ART B predicted by network pharmacological analyses were experimentally validated by real-time PCR and Western blot assays on H1299 cells. Results: UPLC-QTOF-MS/MS identified a total of 69 compounds (such as ART B, mangiferin, and artemisinic acid) in QBD. The in vivo data showed that QBD significantly inhibited the growth of H1299 cells in xenograft larval zebrafish from 125 to 500 µg/mL. The in vitro data showed that QBD induced apoptosis of H1299 cells, accompanied by down-regulating the expression of BCL-2 and up-regulating the expression of BIM, PUMA, BAX, c-PARP, γ-H2A.X, c-CASP3, and c-CASP8. Alike QBD, ART B exerted similar anti-proliferative and pro-apoptotic effects on H1299 cells. Moreover, ART B inhibited expressions of BCL2L1, AKT1, AKT2, MMP-2, and EGFR, and up-regulated ALB expression. Mechanistically, ART B promoted apoptosis of H1299 cells by inhibiting PI3K/Akt signaling pathway. Conclusion: This study revealed the anti-NSCLC efficacy of QBD. ART B, the effective component of QBD, plays an anti-NSCLC role by down-regulating the PI3K-Akt signaling pathway. It suggests that QBD and ART B are promising drug candidates for NSCLC treatment.

Risk factors for cannula-associated arterial thrombosis following extracorporeal membrane oxygenation support: a retrospective study.

BACKGROUND: Hemostatic dysfunction during extracorporeal membrane oxygenation (ECMO) due to blood-circuit interaction and the consequences of shear stress imposed by flow rates lead to rapid coagulation cascade and thrombus formation in the ECMO system and blood vessels. We aimed to identify the incidence and risk factors for cannula-associated arterial thrombosis (CaAT) post-decannulation. METHODS: A retrospective study of patients undergoing arterial cannula removal following ECMO was performed. We evaluated the incidence of CaAT and compared the characteristics, ECMO machine parameters, cannula sizes, number of blood products transfused during ECMO, and daily hemostasis parameters in patients with and without CaAT. Multivariate analysis identified the risk factors for CaAT. RESULTS: Forty-seven patients requiring venoarterial ECMO (VA-ECMO) or hybrid methods were recruited for thrombosis screening. The median Sequential Organ Failure Assessment score was 11 (interquartile range, 8-13). CaAT occurred in 29 patients (61.7%), with thrombosis in the superficial femoral artery accounting for 51.7% of cases. The rate of limb ischemia complications in the CaAT group was 17.2%. Multivariate analysis determined that the ECMO flow rate-body surface area (BSA) ratio (100 ml/min/m2) was an independent factor for CaAT, with an odds ratio of 0.79 (95% confidence interval, 0.66-0.95; P=0.014). CONCLUSIONS: We found that the incidence of CaAT was 61.7% following successful decannulation from VA-ECMO or hybrid modes, and the ECMO flow rate-BSA ratio was an independent risk factor for CaAT. We suggest screening for arterial thrombosis following VA-ECMO, and further research is needed to determine the risks and benefits of such screening.

Sol-Gel Synthesis and Photoluminescence Properties of a Far-Red Emitting Phosphor BaLaMgTaO6:Mn4+ for Plant Growth LEDs.

Far-red (FR) emitting LEDs are known as a promising supplement light source for photo-morphogenesis of plants, in which FR emitting phosphors are indispensable components. However, mostly reported FR emitting phosphors are suffering from problems of wavelength mismatch with LED chips or low quantum efficiency, which are still far from practical applications. Here, a new efficient FR emitting double-perovskite phosphor BaLaMgTaO6:Mn4+ (BLMT:Mn4+) has been prepared by sol-gel method. The crystal structure, morphology and photoluminescence properties have been investigated in detail. BLMT:Mn4+ phosphor has two strong and wide excitation bands in the range of 250-600 nm, which matches well with a near-UV or blue chip. Under 365 nm or 460 nm excitation, BLMT:Mn4+ emits an intense FR light ranging from 650 to 780 nm with maximum emission at 704 nm due to 2Eg → 4A2g forbidden transition of Mn4+ ion. The critical quenching concentration of Mn4+ in BLMT is 0.6 mol%, and its corresponding internal quantum efficiency is as high as 61%. Moreover, BLMT:Mn4+ phosphor has good thermal stability, with emission intensity at 423 K keeping 40% of the room temperature value. The LED devices fabricated with BLMT:Mn4+ sample exhibit bright FR emission, which greatly overlaps with the absorption curve of FR absorbing phytochrome, indicating that BLMT:Mn4+ is a promising FR emitting phosphor for plant growth LEDs.

Gallic acid in theabrownin suppresses cell proliferation and migration in non­small cell lung carcinoma via autophagy inhibition.

The bioactive extract of green tea, theabrownin (TB), is known to exhibit pro-apoptotic and antitumor effects on non-small cell lung cancer (NSCLC). Gallic acid (GA) is a crucial component of TB; however, its mechanism of action in NSCLC has been rarely studied. To date, little attention has been paid to the anti-NSCLC activity of GA. Therefore, the present study investigated the effects of GA in vivo and in vitro. Cell Counting Kit (CCK)-8 assay, DAPI staining and flow cytometry, wound-healing assay and western blotting were used to assess cell viability, apoptosis, migration and protein expression, respectively. In addition, a xenograft model was generated, and TUNEL assay and immunohistochemistry analysis were performed. The CCK-8 data showed that the viability of H1299 cells was significantly inhibited by GA in a dose- and time-dependent manner. DAPI staining, Annexin-V/PI staining and wound-healing data showed that GA exerted pro-apoptotic and anti-migratory effects on H1299 cells in a dose-dependent manner. Furthermore, the results of western blotting showed that GA significantly upregulated the levels of pro-apoptotic proteins [cleaved (c-)PARP, c-caspase8, c-caspase-9 and the ratio of γ-H2A.X/H2A.X]. In vivo data confirmed the antitumor effect of GA through apoptosis induction in an autophagy-dependent manner. In conclusion, the present study confirmed the anti-proliferative, pro-apoptotic and anti-migratory effects of GA against NSCLC in vitro and in vivo, providing considerable evidence for its potential as a novel candidate for the treatment of NSCLC.