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For the past 300 years, hydrogen sulfide (H2S) has been considered a toxic gas. Nowadays, it has been found to be a novel signaling molecule in plants involved in the regulation of cellular metabolism, seed germination, plant growth, development, and response to environmental stresses, including high temperature (HT) and low temperature (LT). As a signaling molecule, H2S can be actively synthesized and degraded in the cytosol, chloroplasts, and mitochondria of plant cells by enzymatic and non-enzymatic pathways to maintain homeostasis. To date, plant receptors for H2S have not been found. It usually exerts physiological functions through the persulfidation of target proteins. In the past 10 years, H2S signaling in plants has gained much attention. Therefore, in this review, based on that same attention, H2S homeostasis, protein persulfidation, and the signaling role of H2S in plant response to HT and LT stress were summarized. Also, the common mechanisms of H2S-induced HT and LT tolerance in plants were updated. These mechanisms involve restoration of biomembrane integrity, synthesis of stress proteins, enhancement of the antioxidant system and methylglyoxal (MG) detoxification system, improvement of the water homeostasis system, and reestablishment of Ca2+ homeostasis and acid-base balance. These updates lay the foundation for further understanding the physiological functions of H2S and acquiring temperature-stress-resistant crops to develop sustainable food and agriculture.
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OBJECTIVE: This study aimed to investigate the incidence of enteral nutrition intolerance (ENI) in patients with sepsis and explore potential risk factors. METHODS: A case-control study was conducted in patients with sepsis who were receiving enteral nutrition (EN) at a tertiary hospital in China. The included patients were divided into the ENI group and the non-ENI group. Univariate and multivariate analyses were performed to identify the risk factors for ENI. RESULTS: A total of 859 patients were included in the study. Among them, 288 (33.53%) patients experienced symptoms of ENI, including diarrhea, vomiting, bloating, and gastric retention. Logistic regression analysis revealed that the Acute Physiology and Chronic Health Evaluation H (APACHE H) score, thoracocentesis, and usage of cardiotonic drugs (namely, inotropes) were independent predictors of the ENI. CONCLUSION: The incidence of ENI is relatively high in patients with sepsis, especially in those who have higher APACHE H scores, have undergone thoracocentesis, and have received inotropes.
Subject(s)
Enteral Nutrition , Sepsis , Humans , Case-Control Studies , Nutritional Status , Sepsis/complications , Sepsis/epidemiology , Risk FactorsABSTRACT
According to research, shock, the most common complication of extremely severe burns, is also the leading cause of mortality among patients with such burns. The case fatality rate reaches 83.45% when the total burn area exceeds 90%. The American Heart Association in 2020 recommended the intraosseous (IO) access after the peripheral access and prior to the central venous access when venous cannulation is either difficult or delayed. The use and experience with intraosseous infusion in extremely severe burns are still limited. We report efficacy and safety results from 19 burn patients treated with IO infusion between June 2020 and December 2022. In these patients, the mean injury time of burns was 1.55 ± 1.10 hours, the mean burn surface area was 86.24% ± 11.33%, the mean catheterization time was 49.68 ± 10.11 seconds, and the mean emergency retention time was 2.75 ± 1.74 hours, the mean actual fluid supplement amount was 5,533.68 ± 3,077.19 mL, the mean hourly urine volume of the patient was 93.31 ± 60.94 mL, the mean emergency detention time was 4.16 ± 2.97 hours, and the mean duration of hospitalization was 34.50 ± 25.38 days. The results demonstrated a clinically meaningful improvement and higher response rate vs peripheral venous cannulation and an acceptable safety profile in those patients.
Subject(s)
Burns , Shock , Humans , Burns/therapy , Infusions, Intraosseous , Fluid Therapy/methods , Resuscitation/methodsABSTRACT
In order to deeply study the basic characteristics, diffusion laws, and flow laws of coal gangue and coal gangue slurry, the basic characteristic parameters of coal gangue and coal gangue slurry were obtained through particle size distribution test, electron microscope scanning test, X-ray diffraction test, X-ray fluorescence spectrum test, and angle of repose test. The conveying performance test of coal gangue slurry was carried out, and based on this, a simulation test of coal gangue slurry caving areas was designed. The diffusion and flow laws of coal gangue slurry under the same inclination angle were summarized, and the field test of fluidization filling in the caving areas was conducted. The results show that: (1) The water-to-gangue ratio was the main controlling factor for the conveying performance of coal gangue slurry. The extensibility, slump, and bleeding rate of the coal gangue slurry increased with the increase of the water-to-gangue ratio. (2) The diffusion profile of coal gangue slurry at different dip angles was arc-shaped, and the diffusion distance of slurry increased with the increase of infiltration time. However, there were differences in the sustained diffusion ability of different dip angles. (3) At the same time interval, the spatial accumulation patterns of scattered gangue in different regions will lead to differences in the diffusion speed of the slurry. (4) Both burying and hanging pipes in the falling area can safely and efficiently fill the gangue slurry. The diffusion distance of the caving areas in the test working face was basically consistent with the diffusion distance of the slurry in the simulation test of the coal gangue slurry caving areas.
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BACKGROUND: Extracorporeal membrane oxygenation (ECMO) has been increasingly used in China, but nosocomial infections (NI) in patients receiving ECMO remain poorly characterized. Thus, this study aimed to investigate the incidence rate, causative was pathogens, and risk factors of NIs in ECMO patients. METHODS: A retrospective cohort study of patients receiving ECMO between January 2015 and October 2021 was conducted in a tertiary hospital. General demographics and clinical data of the included patients were collected from the electronic medical record system and the real-time NI surveillance system. RESULTS: A total of 86 infected patients with 110 episodes of NIs were identified in 196 patients receiving ECMO. The incidence of NI was 59.2/1000 ECMO days. The median time for the first NI in ECMO patients was 5 days (interquartile range: 2-8 days). Hospital-acquired pneumonia and bloodstream infections were common types of NIs in ECMO patients, and the main pathogens were gram-negative bacteria. Pre-ECMO invasive mechanical ventilation (OR = 2.40, 95% CI:1.12-5.15) and prolonged duration of ECMO (OR = 1.26, 95% CI:1.15-1.39) were risk factors for NIs during ECMO support. DISCUSSION: This study identified the main infection sites and pathogens of NIs in ECMO patients. Although NIs may not affect successful ECMO weaning, additional measures should be implemented to reduce the incidence of NI during ECMO support.
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INTRODUCTION: The therapeutic cancer vaccine recombinant Epidermal Growth Factor (EGF)-CRM197 is a novel combined conjugate EGF with CRM197 as a carrier protein. Immunization with the EGF-CRM197 vaccine can induce high levels of neutralizing anti-EGF antibodies that inhibit EGF/EGFR signaling and thereby suppress growth of tumors that rely on this signaling pathway. Herein, we characterize the humoral immune responses elicited by the recombinant EGF-CRM197 vaccine in patients with advanced solid tumors in a phase I clinical trial and assess the safety, tolerability, and immunogenicity of this vaccine (CTR20190473). METHODS: A total of 16 subjects were enrolled in this study. Under 6 + 3 design, patients in each dosing cohort were administrated subcutaneously at a dosage of 0.4 mg, 0.8 mg, and 1.6 mg, respectively. The patients received vaccinations for immune induction (once a week for 4 consecutive weeks) and booster vaccinations (once every 4 weeks). Safety evaluation was performed 1 week after the immune induction. Booster vaccination was given until the occurrence of disease progression, intolerance, withdrawal of informed consent by the patient, or negative result of anti-EGF test after two booster vaccinations. RESULTS: Vaccination with EGF-CRM197 is safe and well-tolerated in patients with advanced solid tumors. Adverse reactions at the injection site were the most common adverse events (AEs) in recipients. No severe adverse reactions post vaccination were observed in the present study. Vaccinated patients developed a robust neutralizing antibody response triggered by EGF-CRM197 that significantly reduced the levels of EGF in serum. For lung cancer patients who were super good antibody responders (sGAR) to EGF-CRM197, the median progress-free survival (PFS) was 4.83 months, significantly longer than that of the good antibody responder (GAR) patients with lung cancer whose median PFS was 2.10 months (P=0.0018). The median overall survival (OS) of GAR lung cancer patients was 10.67 months while the OS) for sGAR lung cancer patients was not reached until analysis was performed. The median follow-up of the sGAR lung cancer patients was 14.6 months. CONCLUSION: Our study demonstrates that the recombinant EGF-CRM197 therapeutic cancer vaccine can induce a good immune response in patients with advanced solid tumors and is safe and well tolerated, which ensures further clinical development of the vaccine for extending the survival time of EGF-CRM197 sensitive patients with advanced solid tumors. CLINICAL TRIAL REGISTRATION: http://www.chinadrugtrials.org.cn, identifier CTR20190473, EGF-CRM197.
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Signal transducer and activator of transcription (STAT)3 expression is correlated with neoplasm growth, metastasis, and prognosis; it has also been implicated in the regulation of autophagy, which may in turn contribute to tumor chemoresistance. However, it is unknown whether STAT3 is involved in cancer cell survival in response to chemotherapy. In this study, we show that autophagy is triggered during chemotherapy and that inhibiting autophagy increased chemosensitivity of castration-resistant prostate cancer (CRPC) cells. Meanwhile, docetaxel induced autophagy was inhibited by STAT3 activation, which increased mitochondrial damage and decreased CRPC cell viability. These results suggest that STAT3 contributes to CRPC cell survival and chemoresistance by modulating autophagy.
Subject(s)
Autophagy/drug effects , Drug Resistance, Neoplasm/drug effects , STAT3 Transcription Factor/antagonists & inhibitors , Taxoids/pharmacology , Antineoplastic Agents/pharmacology , Autophagy/genetics , Cell Line, Tumor , Cell Survival/drug effects , Cell Survival/genetics , Docetaxel , Drug Resistance, Neoplasm/genetics , Gene Expression Regulation, Neoplastic/drug effects , Humans , Male , Prostatic Neoplasms, Castration-Resistant/genetics , Prostatic Neoplasms, Castration-Resistant/metabolism , Prostatic Neoplasms, Castration-Resistant/pathology , STAT3 Transcription Factor/metabolismABSTRACT
Autophagy is a lysosome-dependent process involved in protein and organelle degradation. It has been suggested that autophagy is activated in nutrient-deficient condition and plays an important role in protecting cells from nutrient shortage. However, the effect of autophagy on chemotherapy during nutrient deficiency has been rarely researched. In the present study, we discovered that hepatocarcinoma cells exhibit chemoinsensitivity accompanied by the activation of autophagy when cultured in nutrient-deprived medium. Inhibition of autophagy by 3-methyladenine or siRNAtargeted Beclin 1 increased the nutrient deprivationinduced apoptosis and chemosensitivity in hepatocarcinoma cells. Furthermore, decreased mitochondrial mass was detected when cells underwent autophagy. The present study suggests that induction of autophagy confers a survival advantage for hepatocarcinoma cells during nutrient deprivation, not only rescuing cells from nutrient deficiency-induced cell apoptosis, but also protecting cells from chemotherapy-induced cell death. Combined usage of the inhibition of autophagy and conventional chemotherapeutic agents could be an effective therapy for hepatocarcinoma during nutrient deprivation.
Subject(s)
Adenine/analogs & derivatives , Antineoplastic Agents/pharmacology , Apoptosis Regulatory Proteins/metabolism , Carcinoma, Hepatocellular/drug therapy , Liver Neoplasms/metabolism , Adenine/pharmacology , Apoptosis Regulatory Proteins/genetics , Autophagy/drug effects , Beclin-1/genetics , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/metabolism , Cell Culture Techniques , Cell Line, Tumor , Cell Survival/drug effects , Cisplatin/pharmacology , Fluorouracil/pharmacology , Gene Expression Regulation, Neoplastic/drug effects , Hep G2 Cells , Humans , Liver Neoplasms/drug therapy , Liver Neoplasms/genetics , Membrane Potential, Mitochondrial/drug effects , Mitochondria/metabolismABSTRACT
Germanium Tin (GeSn) films have drawn great interest for their visible and near-infrared optoelectronics properties. Here, we demonstrate large area Germanium Tin nanometer thin films grown on highly flexible aluminum foil substrates using low-temperature molecular beam epitaxy (MBE). Ultra-thin (10-180 nm) GeSn film-coated aluminum foils display a wide color spectra with an absorption wavelength ranging from 400-1800 nm due to its strong optical interference effect. The light absorption ratio for nanometer GeSn/Al foil heterostructures can be enhanced up to 85%. Moreover, the structure exhibits excellent mechanical flexibility and can be cut or bent into many shapes, which facilitates a wide range of flexible photonics. Micro-Raman studies reveal a large tensile strain change with GeSn thickness, which arises from lattice deformations. In particular, nano-sized Sn-enriched GeSn dots appeared in the GeSn coatings that had a thickness greater than 50 nm, which induced an additional light absorption depression around 13.89 µm wavelength. These findings are promising for practical flexible photovoltaic and photodetector applications ranging from the visible to near-infrared wavelengths.
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The objective of this study was to perform a meta-analysis and literature review on the predictive role of vascular endothelial growth factor (VEGF) in prostate cancer. A detailed literature search was performed using PubMed and Embase databases for related research publications written in English. Methodological quality of the studies was also evaluated. Data was collected from studies comparing overall survival (OS), progression-free survival (PFS), disease-free survival (DFS), biomedical failure (BF) and cancer-specific survival (CSS) in patients with elevated VEGF levels and those having lower levels. The hazard ratio (HR) and its 95% confidence interval (CI) were used to assess the strength of associations. A total of 12 studies (n = 1,737) were included in this meta-analysis (4 for OS, 3 for CSS, 2 for DFS, 4 for BF, and 4 for PFS). For OS, DFS and PFS, the pooled HR for VEGF was not statistically significant at 1.30 (95% CI, 0.74-2.29), 0.80 (95% CI, 0.57-1.13) and 1.04 (95% CI, 0.93-1.16), respectively. However, for CSS and BF, the pooled HR was 2.32 (95% CI, 1.20-4.46) and 1.30 (95% CI, 1.06-1.59), respectively. Our results demonstrate that VEGF may have a critical prognostic value in patients with prostatic cancer.
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Several studies have reported that C-reactive protein (CRP), an inflammation biomarker, may be associated with the prognosis of prostate cancer (PCa). The objective of this systematic review is to summarize the predictive role of CRP for survival in PCa as reported in previous studies. Related studies were identified, and evaluated for quality through multiple search strategies. Data was collected from studies comparing overall and cancer-specific survival (CSS) in patients with elevated CRP levels and those having lower levels. However, for progression-free survival (PFS), data were collected according to the log of CRP. The hazard ratio (HR) and its 95% confidence interval (CI) were used to assess the strength of associations. A total of nine studies (n = 1,497) were evaluated in this meta-analysis (five for overall survival (OS), four for CSS and two for PFS). For OS and PFS, the pooled HR of CRP was statistically significant at 1.51 (95% CI, 1.28-1.79) and 1.50 (95% CI, 1.25-1.81), respectively. For CSS, the pooled HR was 1.91 (95% CI, 1.36-2.69) with higher CRP expression in PCa, which strongly indicates poorer survival in PCa. This study demonstrates that CRP may have a critical prognostic value in patients with prostatic cancer.
Subject(s)
Biomarkers, Tumor/blood , C-Reactive Protein/metabolism , Prostatic Neoplasms/blood , Disease-Free Survival , Humans , Inflammation Mediators/blood , Male , Prognosis , Prostatic Neoplasms/therapy , Survival AnalysisABSTRACT
BACKGROUND: The potential prognostic value of human equilibrative nucleoside transporter1 in pancreatic cancer receiving gemcitabine-based chemotherapy is variably reported. OBJECTIVE: The objective of this study was to conduct a systematic review of literature evaluating human equilibrative nucleoside transporter1 expression as a prognostic factor in pancreatic cancer receiving gemcitabine-based chemotherapy and to conduct a subsequent meta-analysis to quantify the overall prognostic effect. METHODS: Related studies were identified and evaluated for quality through multiple search strategies. Only studies analyzing pancreatic cancer receiving gemcitabine-based chemotherapy were eligible for inclusion. Data were collected from studies comparing overall, disease-free and progression-free survival (OS, DFS and PFS) in patients with low human equilibrative nucleoside transporter1 levels and those having high levels. The hazard ratio (HR) and its 95% confidence interval (95%CI) were used to assess the strength of associations. Hazard ratios greater than 1 reflect adverse survival associated with low human equilibrative nucleoside transporter1 levels. RESULTS: A total of 12 studies (nâ=â875) were involved in this meta-analysis (12 for OS, 5 for DFS, 3 for PFS). For overall and disease-free survival, the pooled HRs of human equilibrative nucleoside transporter1 were significant at 2.93 (95% confidence interval [95% CI], 2.37-3.64) and 2.67 (95% CI, 1.87-3.81), respectively. For progression-free survival, the pooled HR in higher human equilibrative nucleoside transporter1 expression in pancreatic cancer receiving gemcitabine-based chemotherapy was 2.76 (95% CI, 1.76-4.34). No evidence of significant heterogeneity or publication bias was seen in any of these studies. CONCLUSION: These results support the case for a low human equilibrative nucleoside transporter1 level representing a significant and reproducible marker of adverse prognosis in pancreatic cancer receiving gemcitabine-based chemotherapy.
Subject(s)
Biomarkers, Tumor/metabolism , Equilibrative Nucleoside Transporter 1/metabolism , Pancreatic Neoplasms/diagnosis , Pancreatic Neoplasms/metabolism , Antineoplastic Agents/therapeutic use , Deoxycytidine/analogs & derivatives , Deoxycytidine/therapeutic use , Humans , Prognosis , Proportional Hazards Models , GemcitabineABSTRACT
BACKGROUND: The UGT1A1*28 polymorphism is known as a biomarker of irinotecan-induced neutropenia in Caucasians. However, in Asians, the UGT1A1*28 mutation is much less frequent. METHODS: A meta-analysis was performed to assess the association of the UGT1A1*6 and UGT1A1*28 with neutropenia in Asians. RESULTS: In a combination test of the two variations, patients with severe neutropenia displayed a 155% higher mutational load than those that were not neutropenic (ORG = 2.55; 95% CI: 1.82-3.58). CONCLUSIONS: In Asians, a combination test of UGT1A1*6 and UGT1A1*28 might be a potential biomarker of irinotecan-induced neutropenia, an observation that will need additional trials for confirmation.
Subject(s)
Antineoplastic Agents, Phytogenic/adverse effects , Camptothecin/analogs & derivatives , Glucuronosyltransferase/genetics , Neutropenia/genetics , Asian People , Camptothecin/adverse effects , Gene Frequency , Genetic Association Studies , Genetic Predisposition to Disease , Humans , Irinotecan , Neutropenia/chemically induced , Polymorphism, Genetic , RiskABSTRACT
OBJECTIVE: To observe the changes in the expressions of STAT3 and NF-KB in PC-3 cells after IL-6 stimulation and to verify the effects of the NF-KB inhibitor caffeic acid phenethyl ester (CAPE) on the expressions of p-STAT3 and IL-6 in the PC-3 prostate cancer cell line. METHODS: PC-3 prostate cancer cells were treated with IL-6 at 20 ng/ml for 5, 10, 20, 30 and 45 min. The protein and mRNA expressions of STAT3 and NF-kappaB were measured by Western blot and real time PCR, respectively, and the cell cycle was detected by flow cytometry. The PC-3 cells were exposed to TNF-alpha or TNF-alpha + CAPE, followed by determination of the IL-6 expression in the supernatant of the cells by ELISA and the expression of p-STAT3 by Western blot. RESULTS: After IL-6 stimulation, both the expression of p-STAT3 protein and the proliferation index of the PC-3 cells were significantly increased, and so were the expressions of IL-6 and p-STAT3 protein in the supernatant after TNF-alpha treatment (P < 0.05). TNF-alpha + CAPE induced statistically lower expressions of IL-6 and p-STAT3 than TNF-alpha alone (P < 0.05). CONCLUSION: CAPE can inhibit IL-6 secretion induced by TNF-alpha in PC-3 cells and thus suppress STAT3 translocation. Therefore, by inhibiting the expression of NF-kappaB and affecting STAT3 and other related cell signaling pathways, CAPE may become a new therapeutic option for prostate cancer.