miR-let-7a inhibits sympathetic nerve remodeling after myocardial infarction by downregulating the expression of nerve growth factor.

Objective: Sympathetic hyperinnervation following myocardial infarction (MI) is one of the primary causes of ventricular arrhythmias (VAs) after MI. Nerve growth factor (NGF) is a key molecule that induces sympathetic nerve remodeling. Previous studies have confirmed that microRNA (miR)-let-7a interacts with NGF. However, whether miR-let-7a is involved in sympathetic remodeling after MI remains unknown. We aimed to investigate whether miR-let-7a was associated with the occurrence of VA after MI. Methods and results: A rat model of myocardial infarction was established using left coronary artery ligation. miR-let-7a expression levels were analyzed by reverse transcription-quantitative PCR. Western blotting was also used to examine NGF expression levels in vivo and in M1 macrophages in vitro. The relationship between miR-let-7a and NGF levels was investigated using a luciferase reporter assay. The results revealed that the expression of miR-let-7a decreased significantly after MI, while NGF expression was significantly upregulated. In addition, overexpression of miR-let-7a effectively inhibited NGF expression in rats, which was also verified in M1 macrophages. Tyrosine hydroxylase and growth-associated protein 43 immunofluorescence results revealed that the administration of a miR-let-7a overexpression lentivirus to rats inhibited sympathetic remodeling after MI. Programmed electrical stimulation, renal sympathetic nerve activity recording, and heart rate variability measurements showed that miR-let-7a overexpression decreased sympathetic activity. Conclusions: These findings provide novel insights into the molecular mechanisms by which miR-let-7a and NGF contribute to the progression of sympathetic nerve remodeling after MI. Therefore, miR-let-7a may be a promising therapeutic target to reduce the incidence of arrhythmia following MI.

Oxytocin Attenuates Sympathetic Innervation with Inhibition of Cardiac Mast Cell Degranulation in Rats after Myocardial Infarction.

Sympathetic hyperinnervation is the leading cause of fatal ventricular arrhythmia (VA) after myocardial infarction (MI). Cardiac mast cells cause arrhythmias directly through degranulation. However, the role and mechanism of mast cell degranulation in sympathetic remodeling remain unknown. We investigated the role of oxytocin (OT) in stabilizing cardiac mast cells and improving sympathetic innervation in rats. MI was induced by coronary artery ligation. Western blotting, immunofluorescence, and toluidine staining of mast cells were performed to determine the expression and location of target protein. Mast cells accumulated significantly in peri-infarcted tissues and were present in a degranulated state. They expressed OT receptor (OTR), and OT infusion reduced the number of degranulated cardiac mast cells post-MI. Sympathetic hyperinnervation was attenuated as assessed by immunofluorescence for tyrosine hydroxylase (TH). Seven days post-MI, the arrhythmia score of programmed electrical stimulation was higher in vehicle-treated rats with MI than in rats treated with OT. An in vitro study showed that OT stabilized mast cells via the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Further in vivo studies on OTR-deficient mice showed worsening mast cell degranulation and worsening sympathetic innervation. OT pretreatment inhibited cardiac mast cell degranulation post-MI and prevented sympathetic hyperinnervation, along with mast cell stabilization via the PI3K/Akt pathway. SIGNIFICANCE STATEMENT: This is the first study to elucidate the role and mechanism of oxytocin (OT) in inflammatory-sympathetic communication mediated sympathetic hyperinnervation after myocardial infarction (MI), providing new approaches to prevent fatal arrhythmias.

Biological fermentation pilot-scale systems and evaluation for commercial viability towards sustainable biohydrogen production.

Featuring high caloric value, clean-burning, and renewability, hydrogen is a fuel believed to be able to change energy structure worldwide. Biohydrogen production technologies effectively utilize waste biomass resources and produce high-purity hydrogen. Improvements have been made in the biohydrogen production process in recent years. However, there is a lack of operational data and sustainability analysis from pilot plants to provide a reference for commercial operations. In this report, based on spectrum coupling, thermal effect, and multiphase flow properties of hydrogen production, continuous pilot-scale biohydrogen production systems (dark and photo-fermentation) are established as a research subject. Then, pilot-scale hydrogen production systems are assessed in terms of sustainability. The system being evaluated, consumes 171,530 MJ of energy and emits 9.37 t of CO2 eq when producing 1 t H2, and has a payback period of 6.86 years. Our analysis also suggests future pathways towards effective biohydrogen production technology development and real-world implementation.

Investigation on the mechanism of the combination of eremias multiocellata and cisplatin in reducing chemoresistance of gastric cancer based on in vitro and in vivo experiments.

BACKGROUND: Cisplatin (DDP) is one of the important chemotherapy drugs for patients with advanced gastric cancer and metastasis, but its resistance is a bottleneck problem that affects clinical efficacy and patient survival. Eremias multiocellata (EM) is a traditional Chinese herbal medicine, which has been used in the treatment of precancerous lesions, gastric cancer, liver fibrosis, and other digestive diseases. However, the mechanism of reducing chemotherapy resistance to gastric cancer is still unclear. METHODS: We used the MTT assay to evaluate the proliferative viability of gastric cancer parental cell line MKN45 and its drug-resistant cell line MKN45/DDP, and compared their drug-resistance indices. The migration and invasion abilities of MKN45/DDP drug-resistant cells were evaluated using the Transwell assay. Apoptosis in MKN45/DDP drug-resistant cells was detected using flow cytometry. The effect of a combination of EM and cisplatin on the levels of reactive oxygen species (ROS) and lipid peroxides (LPO) in cisplatin-resistant gastric cancer cells was detected using ROS fluorescent probes and a lipid peroxidation assay kit in conjunction with flow cytometry. The effect of EM combined with cisplatin on the level of iron ions was detected by fluorescence probe and confocal laser technique. Hematoxylin-eosin staining (HE staining) was used to detect the histopathologic morphology of drug-resistant gastric cancer in nude mice. Ferroptosis-related proteins were measured using immunohistochemistry. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect tumor drug resistance-related genes. The NF-κB/Snail pathway-related proteins, PI3K/AKT/mTOR pathway-related proteins, and drug resistance-related proteins were detected by Western blot. RESULTS AND CONCLUSIONS: The results of in vitro and in vivo experiments showed that EM combined with DDP could effectively inhibit the migration and invasive ability of MKN45/DDP cells, as well as induce apoptosis of MKN45/DDP cells; the combination of the two drugs could significantly increase the levels of ROS, lipid peroxidation and divalent ferric ions in MKN45/DDP cells, at the same time reducing the levels of Ferroptosis-related proteins, which could induce Ferroptosis. In addition, EM combined with DDP can also exert the effect of reversing DDP resistance and increasing the sensitivity of gastric cancer drug-resistant cells to DDP by regulating the NF-κB/Snail signaling pathway, PI3K/AKT/mTOR signaling pathway, and the expression of drug resistance-related proteins and genes.

m6A methyltransferase METTL3 contributes to sympathetic hyperactivity post-MI via promoting TRAF6-dependent mitochondrial ROS production.

OBJECTIVES: N6-methyladenosine (m6A) is the most prevalent post-translational modification in eukaryotic mRNA. Recently, m6A editing modified by methyltransferase-like enzyme 3 (METTL3), the core m6A methyltransferase, has been demonstrated to be involved in cardiac sympathetic hyperactivity. This study aimed to clarify the effects and underlying mechanisms of METTL3 in the paraventricular nucleus (PVN) in mediating sympathetic activity following myocardial infarction (MI). METHODS: We established rat MI models by left anterior descending coronary artery ligation. m6A quantification was performed.The expression of METTL3 and its downstream gene, tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6), were determined. The functional role of METTL3 in sympathetic hyperactivity and electrical conduction stability were verified by assessing renal sympathetic nerve activity (RSNA), norepinephrine (NE) levels, and programmed electrical stimulation. Rescue experiments were also conducted. The mechanism by which m6A is involved in mitochondrial reactive oxygen species (mROS) production, mediated by TRAF6/ECSIT pathway, was explored in lipopolysaccharide (LPS) treated primary microglial cells. RESULTS: METTL3 was predominantly localized in the microglia and significantly increased within the PVN at 3 days post-MI. Inhibition of METTL3 decreased m6A levels, TRAF6 expression, and mROS production; downregulated sympathoexcitation, indicated by attenuated NE concentration and RSNA; decreased the incidence of ventricular tachycardia or fibrillation; and improved cardiac function. Mechanistically, downregulation of METTL3 prevented TRAF6 translocation to the mitochondria in the microglia and subsequent TRAF6/ECSIT pathway activation, resulting in decreased mROS production. CONCLUSIONS: This study demonstrates that METTL3-mediated m6A modification promotes sympathetic hyperactivity through TRAF6/ECSIT pathway and mitochondrial oxidative stress in the PVN, thereby leading to ventricular arrhythmias post-MI.

Malat1 promotes macrophage-associated inflammation by increasing PPAR-γ methylation through binding to EZH2 in acute myocardial infarction.

The inflammatory microenvironment of macrophage plays an important role in acute myocardial infarction (AMI), but the regulatory mechanism is unknown. Here, we aimed to investigate the role of Malat1 on inflammation microenvironment of macrophage in AMI. Our study found that Malat1 expression was increased in AMI, which mainly expressed in macrophages. Malat1 inhibition improved collagen deposition and inflammation in infarcted heart. In vitro, Malat1 inhibition evidently reduced macrophage-associated inflammation. The results from ribonucleic acid pull-down (RNA pull-down) and RNA Immunoprecipitation (RIP) assay demonstrated that Malat1 directly binds to EZH2. Malat1 and EZH2 complex could increase histone H3K27me3 expression and further inhibit the production of PPAR-γ. In vivo, inhibition of Malat1 also leaded to the down-regulation of both EZH2 and H3K27me3, as well as up-regulation of PPAR-γ in infarcted heart. Therefore, these findings demonstrate a novel mechanism of Malat1 on inflammation microenvironment of macrophage in AMI, which provide a new target for its treatment.

Effect of deep eutectic solvent pretreatment on biohydrogen production from corncob: pretreatment temperature and duration.

Deep eutectic solvent pretreatment with different temperatures and durations was applied to corncob to increase hydrogen yield via photo-fermentation. The correlation of composition, enzymatic hydrolysis, and hydrogen production in pretreated corncobs, as well as energy conversion was evaluated. Deep eutectic solvent pretreatment effectively dissolved lignin, retained cellulose, and enhanced both enzymatic hydrolysis and hydrogen production. The maximum cumulative hydrogen yield obtained under a pretreatment condition of 50°C and 12 h was 677.45 mL; this was 2.72 times higher than that of untreated corncob, and the corresponding lignin removal and enzymatic reduction of sugar concentration were 79.15% and 49.83 g/L, respectively; the highest energy conversion efficiency was 12.08%. The hydrogen production delay period was shortened, and the maximum shortening time was 18.9 h. Moreover, the cellulose content in pretreated corncob was positively correlated with both reducing sugar concentration and hydrogen yield and had the strongest influence on hydrogen production.

Managing Cancer and Living Meaningfully (CALM) alleviates chemotherapy related cognitive impairment (CRCI) in breast cancer survivors: A pilot study based on resting-state fMRI.

BACKGROUND: Chemotherapy related cognitive impairment (CRCI) is a type of memory and cognitive impairment induced by chemotherapy and has become a growing clinical problem. Breast cancer survivors (BCs) refer to patients from the moment of breast cancer diagnosis to the end of their lives. Managing Cancer and Living Meaningfully (CALM) is a convenient and easy-to-apply psychological intervention that has been proven to improve quality of life and alleviate CRCI in BCs. However, the underlying neurobiological mechanisms remain unclear. Resting-state functional magnetic resonance imaging (rs-fMRI) has become an effective method for understanding the neurobiological mechanisms of brain networks in CRCI. The fractional amplitude of low-frequency fluctuations (fALFF) and ALFF have often been used in analyzing the power and intensity of spontaneous regional resting state neural activity. METHODS: The recruited BCs were randomly divided into the CALM group and the care as usual (CAU) group. All BCs were evaluated by the Functional Assessment of Cancer Therapy Cognitive Function (FACT-Cog) before and after CALM or CAU. The rs-fMRI imaging was acquired before and after CALM intervention in CALM group BCs. The BCs were defined as before CALM intervention (BCI) group and after CALM intervention (ACI) group. RESULTS: There were 32 BCs in CALM group and 35 BCs in CAU group completed the overall study. There were significant differences between the BCI group and the ACI group in the FACT-Cog-PCI scores. Compared with the BCI group, the ACI group showed lower fALFF signal in the left medial frontal gyrus and right sub-gyral and higher fALFF in the left occipital_sup and middle occipital gyrus. There was a significant positive correlation between hippocampal ALFF value and FACT-Cog-PCI scores. CONCLUSIONS: CALM intervention may have an effective function in alleviating CRCI of BCs. The altered local synchronization and regional brain activity may be correlated with the improved cognitive function of BCs who received the CALM intervention. The ALFF value of hippocampus seems to be an important factor in reflect cognitive function in BCs with CRCI and the neural network mechanism of CALM intervention deserves further exploration to promote its application.

FURIN suppresses the progression of atherosclerosis by promoting macrophage autophagy.

FURIN, a member of the mammalian proprotein convertases (PCs) family, can promote the proteolytic maturation of proproteins. It has been shown that FURIN plays an important role in the progression of atherosclerosis (AS). Current evidence indicates that autophagy widely participates in atherogenesis. This study aimed to explore whether FURIN could affect atherogenesis via autophagy. The effect of FURIN on autophagy was studied using aortic tissues from aortic dissection patients who had BENTALL surgery, as well as macrophages and ApoE-/- mice. In atherosclerotic plaques of aortic tissues from patients, FURIN expression and autophagy were elevated. In macrophages, FURIN-shRNA and FURIN-overexpression lentivirus were used to intervene in FURIN expression. The results showed that FURIN overexpression accelerated LC3 formation in macrophages during the autophagosome formation phase. Furthermore, FURIN-induced autophagy resulted in lower lipid droplet concentrations in macrophages. The western blot revealed that FURIN regulated autophagy via the AMPK/mTOR/ULK1/PI3KIII signaling pathway. In vivo, FURIN overexpression resulted in increased macrophage LC3 formation in ApoE-/- mice atherosclerotic plaques, confirming that FURIN could inhibit the progression of AS by promoting macrophage autophagy. The present study demonstrated that FURIN suppressed the progression of AS by promoting macrophage autophagy via the AMPK/mTOR/ULK1/PI3KIII signaling pathway, which attenuated atherosclerotic lesion formation. Based on this data, current findings add to our understanding of the complexity of AS.

Psychological distress is involved in CRCI in breast cancer survivors via mediating cytokine levels.

BACKGROUND: Cancer-related cognitive impairment (CRCI) is a frequent consequence in breast cancer survivors after chemotherapy and lowers their quality of life (QOL). Psychological distress is frequently experienced by breast cancer survivors. There are currently few studies investigating the role of psychological distress in the genesis of CRCI. METHODS: In total, 122 breast cancer survivors after standard chemotherapy within a year were recruited and assessed using the Psychological Distress Thermometer (DT). Sixty breast cancer survivors had non-psychological distress (NPD group) and sixty-two breast cancer survivors with psychological distress (PD group). The scores of the Mini-Mental State Examination (MMSE), prospective and retrospective memory (PM and RM) Questionnaire (PRMQ), and Functional Assessment of Cancer Therapy-General (FACT-G) and the levels of cytokines including interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), and interleukin-4 (IL-4) were compared between the two groups. Using PROCESS, we investigated whether psychological distress predicted cognitive function based on MMSE through IL-1ß, TNF-α, and IL-4. RESULTS: The PD group had higher scores on RM, PM, and FACT-G and lower scores on MMSE than the NPD group (t = -11.357, t = -10.720, t = -15.419, t = 10.162, respectively; p < 0.05). Meanwhile, a higher level of IL-1ß, TNF-α, and IL-4 was observed in the PD group than in the NPD group (t = -3.961, t = -3.396, t = -3.269, respectively; p < 0.05). The link between psychological distress and cognitive function as measured by the MMSE was also mediated by IL-1ß, TNF-α, and IL-4 (effect size: 26%, 25%, and 24%). CONCLUSION: Breast cancer patients with psychological distress displayed poor cognitive function, poor memory, and inferior quality of life, which was accompanied by higher cytokine levels of IL-1ß, TNF-α, and IL-4. This study demonstrated IL-1ß, TNF-α, and IL-4 as potential pathways to CRCI in response to ongoing psychological distress, which provided evidence for the involvement of psychological distress in CRCI in breast cancer survivors.

A comprehensive computational analysis to explore the importance of SIGLECs in HCC biology.

BACKGROUND: Hepatocellular carcinoma (HCC) is an aggressive, malignant cancer with a complex pathogenesis. However, effective therapeutic targets and prognostic biomarkers are limited. Sorafenib provides delaying cancer progression and survival improvement in advanced HCC. But despite 10 years of research on the clinical application of sorafenib, predictive markers for its therapeutic effect are lacking. METHODS: The clinical significance and molecular functions of SIGLEC family members were assessed by a comprehensive bioinformatic analysis. The datasets included in this study (ICGC-LIRI-JP, GSE22058 and GSE14520) are mainly based on patients with HBV infections or HBV-related liver cirrhosis. The TCGA, GEO, and HCCDB databases were used to explore the expression of SIGLEC family genes in HCC. The Kaplan-Meier Plotter database was used to evaluate relationships between the expression levels of SIGLEC family genes and prognosis. Associations between differentially expressed genes in the SIGLEC family and tumour-associated immune cells were evaluated using TIMER. RESULTS: The mRNA levels of most SIGLEC family genes were significantly lower in HCC than in normal tissues. Low protein and mRNA expression levels of SIGLECs were strongly correlated with tumour grade and clinical cancer stage in patients with HCC. Tumour-related SIGLEC family genes were associated with tumour immune infiltrating cells. High SIGLEC expression was significantly related to a better prognosis in patients with advanced HCC treated with sorafenib. CONCLUSIONS: SIGLEC family genes have potential prognostic value in HCC and may contribute to the regulation of cancer progression and immune cell infiltration. More importantly, our results revealed that SIGLEC family gene expression may be used as a prognostic marker for HCC patients treated with sorafenib.

Impact of the CALM intervention on breast cancer patients during the COVID-19 pandemic.

OBJECTIVE: The COVID-19 outbreak has adversely affected breast cancer patients both physically and mentally. Managing Cancer and Living Meaningfully (CALM) is a psychological intervention that is easy to implement. It also decreases the possibility of virus transmission because it can be administered online. Therefore, this study investigated the effects of CALM on the sleep quality, memory, psychological distress, and quality of life (QoL) of breast cancer patients during the ongoing COVID-19 pandemic. METHODS: Sixty breast cancer patients were recruited and randomly assigned to a CALM group and a Care as Usual (CAU) group. They filled in questionnaires before and after the CALM intervention and CAU. These included the Sleep Quality Scale (SQS), Prospective Memory Scale (PM), Retrospective Memory Scale (RM), Psychological Distress Thermometer (DT), and Quality of life (QoL) Scale. RESULTS: The scores of all the aforementioned scales after the CALM intervention (ACM) were significantly lower compared to the said scores before the CALM intervention (BCM) and after Care as Usual (ACU) (t = 12.369/8.013, t = 8.632/4.583, t = 7.500/6.900, t = 12.479/9.780, t = 12.224/6.729 respectively, P < 0.05) There was a linear correlation between the QoL, DT, and SQS scores. CONCLUSION: CALM is an effective psychotherapy for breast cancer patients, especially during the COVID-19 pandemic, for improving the QoL because it relieves psychological distress and enhances sleep quality.

Psychological distress as risk factor for the efficacy of whole-brain radiotherapy in brain metastasis patients.

Aim: To evaluate the relationship between psychological distress and the efficacy of whole-brain radiotherapy (WBRT) in advanced brain metastasis patients. Methods: Brain metastasis patients (40 with psychological distress and 47 without psychological distress) completed distress thermometer tests before WBRT, and progression-free survival (PFS) was acquired during the follow-up period. Results: Psychological distress was a risk factor for poorer PFS in patients treated with WBRT (p < 0.01). The PFS of survivors who underwent WBRT was superior for those without psychological distress (hazard ratio: 0.295; 95% CI: 0.173-0.500; p < 0.01). Conclusion: The survival of brain metastasis patients receiving WBRT was influenced by psychological distress, which negatively affected the treatment outcome and is likely to be a potential risk indicator in advanced cancer patients receiving WBRT.

Distress thermometer tests were carried out 1 week before whole-brain radiotherapy to assess psychological distress in 87 brain metastasis patients. The results demonstrated that the progression-free survival of brain metastasis patients with psychological distress was obviously inferior to that of patients without psychological distress. The negative effects of psychological distress could be recognized in advanced patients with brain metastases after whole-brain radiotherapy. Psychological distress is likely to be a potential risk indicator for radiotherapy in brain metastasis patients.

The correlations between psychological distress, cognitive impairment and quality of life in patients with brain metastases after whole-brain radiotherapy.

BACKGROUND: Psychological distress and cognitive impairment are highly prevalent among patients with brain metastases after whole-brain radiotherapy (WBRT). Our purpose was to evaluate the correlations between psychological distress, cognitive impairment and quality of life in patients with brain metastases after WBRT. METHODS: Seventy-one patients with brain metastasis treated with WBRT were enrolled in this study and were investigated with several scales, including the Montreal Cognitive Assessment Scale (MoCA), the Functional Assessment of Cancer Therapy-Cognitive Function version 3 (FACT-Cog, version 3), the Functional Assessment of Cancer Therapy-Brain Module version 4 (FACT-Br, version 4) and the Psychological Distress Thermometer (DT), before and after WBRT. RESULTS: The MoCA, FACT-Cog and FACT-Br scores in patients with brain metastases were significantly decreased after WBRT compared with before WBRT (z = - 7.106, - 6.933 and - 6.250, respectively, P < 0.001), while the DT scores were significantly increased (z = 6.613, P < 0.001). There was an obvious negative correlation between the DT score and the FACT-Cog score (r = - 0.660, P < 0.001), a significant negative correlation between the DT score and the FACT-Br score (r = - 0.833, P < 0.001), and an obvious positive correlation between the FACT-Cog score and the FACT-Br score (r = 0.603, P < 0.001). These results suggest that WBRT can cause cognitive impairment in patients with brain metastases, increase their psychological distress and reduce their quality of life (QOL). CONCLUSION: After receiving WBRT, the cognitive function and QOL of patients with brain metastases were decreased, while psychological distress increased. The cognitive impairment and the decline of QOL after WBRT are associated with increased psychological distress, and that the decline of QOL is associated with cognitive impairment of patients.

Aldehyde dehydrogenase 2 polymorphism is associated with chemotherapy-related cognitive impairment in patients with breast cancer who receive chemotherapy.

BACKGROUND: Chemotherapy-related cognitive impairment (CRCI) is a common but easily overlooked condition that markedly affects the quality of life (QOL) of patients with breast cancer. The rs671 is a common gene polymorphism of aldehyde dehydrogenase 2 (ALDH2) in Asia that is involved in aldehyde metabolism and may be closely related to CRCI. However, no study has yet summarised the association between ALDH2 and CRCI. METHODS: This study enrolled one hundred and twenty-four patients diagnosed with breast cancer according to the pathology results, genotyped for ALDH2 single-nucleotide polymorphisms (SNP) to explore these. The mini-mental state exam (MMSE), verbal fluency test (VFT), and digit span test (DST) results were compared in these patients before and after chemotherapy (CT). RESULTS: We found that patients with ALDH2 gene genotypes of rs671_GG, rs886205_GG, rs4648328_CC, and rs4767944_TT polymorphisms were more likely to suffer from cognitive impairment during chemotherapy. A trend toward statistical significance was observed for rs671_GG of DST (z = 2.769, p = 0.006), VFT (t = 4.624, P<0.001); rs886205_GG of DST (z = 3.663, P<0.001); rs4648328_CC of DST (z = 2.850, p = 0.004), VFT (t = 3.477, p = 0.001); and rs4767944_TT of DST (z = 2.967, p = 0.003), VFT (t = 2.776, p = 0.008). The cognitive indicators of these patients significantly decreased after chemotherapy (p < 0.05). The difference in ALDH2 rs671 was most obvious. CONCLUSION: Our results showed what kinds of ALDH2 genotyped patients that are more likely to develop CRCI. In the future, it may be possible to infer the risk of CRCI by detecting the single-nucleotide locus of ALDH2 that is conducive to strengthening clinical interventions for these patients and improving their QOL. More importantly, this study has important implications for Asian women with breast cancer as ALDH2 rs671 is a common polymorphism in Asians.

The Removal of Cr(VI) from Aqueous Solutions with Corn Stalk Biochar.

The discharge of wastewater containing hexavalent chromium (Cr(VI)) into the environment is very harmful to living things. Therefore, before effluent that contains Cr(VI) can be discharged into the environment, this toxin should be removed from the contaminated water. In this study, corn stalk biochar was investigated to evaluate the Cr(VI) removal efficiency from an aqueous solution. The effects of pH (2-10), biochar concentration (0.5 to 10 g/L), Cr(VI) concentration (10-500 mg/L), and contact time (10-1440 min) were studied. The actual experimental value of the Cr(VI) removal efficiency was 28.67%, largely consistent with the predicted model value of 29.31%, under the optimal conditions of a Cr(VI) concentration of 60 g/L, pH 4, contact time of 270 min, and a biochar concentration of 4.5 g/L. A significant interaction between the Cr(VI) concentration and pH was observed, along with significance in the interaction between Cr(VI) concentration and biochar concentration, which had a greater impact on the removal of Cr(VI). Biosorption onto corn stalk biochar is an affordable and economical adsorption process to treat wastewater contaminated with Cr(VI). The aim of this study is to provide data to serve as a basis for future studies on the use of raw agricultural waste to remove Cr(VI).

Fear of cancer recurrence is related to the efficacy of immunotherapy and quality of life in patients with NSCLC during the COVID-19 pandemic in China.

The outbreak of the COVID-19 pandemic has greatly impacted patients with non-small cell lung cancer (NSCLC), making the fear of cancer recurrence (FCR) more pronounced. We explored the effects of FCR on immunotherapy efficacy and quality of life during the COVID-19 pandemic in China among the 124 NSCLC patients enrolled in this study. Quality of life and immunotherapy efficacy were compared between high- and low-FCR groups after completing 4-6 courses of treatment or cancer progression. Worse immunotherapy efficacy and quality of life were reported for the high-FCR group than for the low-FCR group. These findings emphasize the need to pay close attention to the level of FCR in NSCLC patients. Efforts should be taken to alleviate FCR levels among NSCLC patients. Moreover, research is needed to investigate the possible link between immunotherapy efficacy and FCR.

The correlation between neutrophil-to-lymphocyte ratio, carcinoembryonic antigen, and carbohydrate antigen 153 levels with chemotherapy-related cognitive impairment in early-stage breast cancer patients.

Background: The changes in inflammation and tumor biomarkers are associated with the anti-tumor immunological processes. Early detection and intervention are of great significance to the clinical management of cancer-related diseases. Peripheral blood biomarkers [e.g., neutrophil-to-lymphocyte ratio (NLR), carcinoembryonic antigen (CEA), and carbohydrate antigen 153 (CA153)] are obtained in real-timely, conveniently, and less invasively, and proved to availably predicted the disease states and prognosis of various cancers, including breast cancer (BC). Inflammation and poor disease management promote cognitive impairment. Chemotherapy-related cognitive impairment (CRCI) hazard long-term survival and quality of life (QOL) of BC patients, but its correlation with NLR, CEA, and CA153 is not clear. Purpose: This study aimed to investigate changes in NLR, CEA, and CA153 levels before and after chemotherapy and their correlation with CRCI in patients with early-stage BC. Materials and methods: The 187 patients with BC who were measured for NLR, CEA, and CA153 values within the first 24 hours of admission, were assigned into two groups: the before/after chemotherapy group (BCG/ACG). The ACG was assigned into two subgroups based on the cognitive assessment results: the cognitive normal/impaired group (CNG/CIG). Patients' self-perceived cognitive impairments were evaluated using a mini-mental state examination (MMSE), prospective and retrospective memory (PM and RM) questionnaire (PRMQ), and functional assessment of cancer therapy-cognitive function version 3 (FACT-Cog, version 3, including CogPCI, CogOth, CogPCA, and CogQOL). Their QOL was also evaluated. Results: The NLR and CA153 levels were elevated after chemotherapy (BCG vs ACG: Z = -1.996 and -1.615, P = 0.046 and 0.106, respectively), and significantly elevated in patients with CRCI (BCG vs CIG: Z = -2.444 and -2.293, P = 0.015 and 0.022; respectively). However, there was not reach significant difference in CEA levels between the four groups. In addition, there was a weak to moderate correlation between peripheral blood biomarkers (NLR, CEA, and CA153) levels and CRCI (r = -0.404, -0.205, -0.322; respectively; P < 0.001). Cognitive impairment scores (MMSE, PM, RM, and FACT-Cog) had a strong correlation with QOL in patients with early-stage BC (r = -0.786, 0.851, 0.849, and 0.938; respectively; P < 0.001). Conclusion: NLR and CA153 m be valuable diagnostic adjuncts of CRCI, and CRCI has a strong correlation with QOL in patients with early-stage BC.

Effect of depression disorder on the efficacy and quality of life of first-line chemotherapy combined with immunotherapy in oncogene-driver negative NSCLC patients.

Objective: The current research was to assess the relevance between depression disorder and first-line chemotherapy combined with immunotherapy, quality of life in patients with oncogene-driver negative non-small cell cancer (NSCLC). Methods: NSCLC patients (33 with depression disorder and 34 with no depression disorder) who was received first-line chemotherapy combined with immunotherapy performed Zung Self-rating Depression Scale (SDS) and European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30). Results: The Progression-Free Survival (PFS) of depression disorder group survivors were lower than these of no depression disorder group survivors (HR, 0.352; 95% CI, 0.201-0.617; P<0.05). The statistical significant was revealed about the Objective Response Rate (ORR) and Disease Control Rate (DCR) in two groups (P<0.05). The quality of life scores of NSCLC patients in no depression disorder group was significantly higher after chemotherapy combined with immunotherapy, and manifested as 92.7 ± 28 vs. 76.3 ± 23.3 (t=8.317, P<0.05), and had a significant difference. Conclusion: Depression disorder in oncogene-driver negative NSCLC patients influence the curative effect of chemotherapy combined with immunotherapy, and depression disorder was significantly negatively associated with quality of life following chemotherapy combined with immunotherapy.

Managing cancer and living meaningfully (CALM) as an intervention for severe fatigue in gastrointestinal cancer survivors.

This study aimed to evaluate the effectiveness and feasibility of CALM (managing cancer and living meaningfully), which is a psychotherapeutic intervention used to reduce cancer-related fatigue (CRF) and improve quality of life (QOL) in Chinese gastrointestinal cancer survivors (GCs). A total of 115 GCs were enrolled in this study. All patients were randomly assigned to either the CALM group or the usual care (UC) group. All patients were evaluated using the Piper Fatigue Scale (PFS) and Quality of Life Assessment Scale before and after 2, 4, and 6 CALM or UC sessions with GCs presenting with severe fatigue. We compared the differences in these scores between the CALM group and the UC group and analyzed the correlations between CRF and QOL scores. Compared with the UC group, the CALM group showed significant differences in total CRF, behavioral/daily life CRF, emotional/affective CRF, sensory/physical CRF, cognitive CRF and QOL scores before and after 2, 4, and 6 CALM sessions (F=3106.434, F=1113.831, F=1159.919, F=1502.266, F=820.275, F=606.513, respectively; P<0.001). Finally, negative correlations were found between CRF and QOL scores in the GCs in the CALM group (before treatment: r=-0.46, P=0.0002; after 2 sessions: r=-0.46, P=0.0002; after 4 sessions: r=-0.51, P<0.0001; after 6 sessions: r =-0.44, P=0.0004). The CALM intervention effectively reduced fatigue in cancer patients and improved their QOL. This study suggests that CALM as a psychotherapeutic intervention may be an effective way to reduce CRF.