Combining large-spot low-fluence 1064-nm and fractional 1064-nm picosecond lasers for promoting protective melanosome autophagy via the PI3K/Akt/mTOR signalling pathway for the treatment of melasma.

Melasma is a common condition of hyperpigmented facial skin. Picosecond lasers are reported to be effective for the treatment of melasma. We aimed to identify the most effective therapeutic mode and elucidate the potential molecular mechanisms of picosecond lasers for the treatment of melasma. Female Kunming mice with melasma-like conditions were treated using four different picosecond laser modes. Concurrently, in vitro experiments were conducted to assess changes in melanin and autophagy in mouse melanoma B16-F10 cells treated with these laser modes. Changes in melanin in mouse skin were detected via Fontana-Masson staining, and melanin particles were evaluated in B16-F10 cells. Real-time polymerase chain reaction and western blotting were used to analyse the expression levels of melanosome and autophagy-related messenger ribonucleic acid (mRNA) and proteins. A combination of large-spot low-fluence 1064-nm and fractional 1064-nm picosecond lasers resulted insignificant decreases in melanin as well as in mRNA and protein expression of melanin-synthesizing enzymes (TYR, TRP-1 and MITF). This combination also led to increased expression of the autophagy-related proteins, Beclin1 and ATG5, with a marked decrease in p62 expression. Intervention with the PI3K activator, 740 Y-P, increased TYR, TRP-1, MITF, p-PI3K, p-AKT, p-mTOR and p62 expression but decreased the expression of LC3, ATG5 and Beclin1. A combination of large-spot low-fluence 1064-nm and fractional 1064-nm picosecond lasers proved more effective and safer. It inhibits melanin production, downregulates the PI3K/AKT/mTOR pathway, enhances melanocyte autophagy and accelerates melanin metabolism, thereby reducing melanin content.

Association of Vascular Calcification with Serum lncRNA H19 and Runx2 mRNA Expression in Patients with Uremia.

Background: The objective of this study was to investigate the relationship between vascular calcification, serum lncRNA H19, and Runt-Related Transcription Factor 2 mRNA expression in patients with uremia. Methods: This study is a retrospective study which recruited 146 patients with uremia on dialysis from December 2021 to November 2022. Participants were divided into the VC and non-VC groups based on their chest X-ray calcification ratings. General and clinical data were collected from all patients. Serum H19, Runx2 mRNA, mineral bone disease effectors, and other blood markers were tested. Univariate analysis was performed to compare the changes in each clinical index between these two groups of patients. A multi-factor logistic regression analysis of risk factors for VC was performed. Receiver operating characteristics analyzed the H19 and Runx2 for their diagnostic values for VC. Pearson's test was used to analyze the correlation between the H19 and Runx2 expression and the factors influencing VC. Results: Patients in the VC group had significantly higher creatinine, serum phosphorus, calcium, BMP-2, FGF-23, OPG, and iPTH levels than those in the non-VC group (P < .05), while their albumin levels were significantly lower than those in the non-VC group (P < .05). The expression of H19 and Runx2 mRNA was significantly upregulated in the serum of VC patients (P < .05). H19 was significantly positively correlated with creatinine, serum phosphorus, calcium, BMP-2, OPG, and iPTH (P < .05). Runx2 mRNA was significantly positively correlated with creatinine, FGF-23, and iPTH (P < .05 ), while there was no significant correlation with other factors(P > .05). Albumin, BMP-2, iPTH, H19, and Runx2 were independent correlative-factors of uremic VC. In addition, the combined H19 and Runx2 test (AUC=0.850; 95% CI: 0.781-0.903) had good diagnostic values for the development of VC. Conclusion: Serum H19 and Runx2 levels are significantly associated with VC-related factors and are independent risk factors for uremic VC, and their levels contribute to the diagnosis of uremic VC.

Integrated multi-omics analysis and machine learning developed a prognostic model based on mitochondrial function in a large multicenter cohort for Gastric Cancer.

BACKGROUND: Gastric cancer (GC) is a common and aggressive type of cancer worldwide. Despite recent advancements in its treatment, the prognosis for patients with GC remains poor. Understanding the mechanisms of cell death in GC, particularly those related to mitochondrial function, is crucial for its development and progression. However, more research is needed to investigate the significance of the interaction between mitochondrial function and GC cell death. METHODS: We employed a robust computational framework to investigate the role of mitochondria-associated proteins in the progression of GC in a cohort of 1,199 GC patients. Ten machine learning algorithms were utilized and combined into 101 unique combinations. Ultimately, we developed a Mitochondrial-related-Score (MitoScore) using the machine learning model that exhibited the best performance. We observed the upregulation of LEMT2 and further explored its function in tumor progression. Mitochondrial functions were assessed by measuring mitochondrial ATP, mitochondrial membrane potential, and levels of lactate, pyruvate, and glucose. RESULTS: MitoScore showed significant correlations with GC immune and metabolic functions. The higher MitoScore subgroup exhibited enriched metabolic pathways and higher immune activity. Overexpression of LETM2 (leucine zipper and EF-hand containing transmembrane protein 2) significantly enhanced tumor proliferation and metastasis. LETM2 plays a role in promoting GC cell proliferation by activating the mTOR pathway, maintaining mitochondrial homeostasis, and promoting glycolysis. CONCLUSION: The powerful machine learning framework highlights the significant potential of MitoScore in providing valuable insights and accurate assessments for individuals with GC. This study also enhances our understanding of LETM2 as an oncogene signature in GC. LETM2 may promote tumor progression by maintaining mitochondrial health and activating glycolysis, offering potential targets for diagnosis, treatment, and prognosis of GC.

Circulating miR-129-3p in combination with clinical factors predicts vascular calcification in hemodialysis patients.

Background: Vascular calcification (VC) commonly occurs and seriously increases the risk of cardiovascular events and mortality in patients with hemodialysis. For optimizing individual management, we will develop a diagnostic multivariable prediction model for evaluating the probability of VC. Methods: The study was conducted in four steps. First, identification of miRNAs regulating osteogenic differentiation of vascular smooth muscle cells (VSMCs) in calcified condition. Second, observing the role of miR-129-3p on VC in vitro and the association between circulating miR-129-3p and VC in hemodialysis patients. Third, collecting all indicators related to VC as candidate variables, screening predictors from the candidate variables by Lasso regression, developing the prediction model by logistic regression and showing it as a nomogram in training cohort. Last, verifying predictive performance of the model in validation cohort. Results: In cell experiments, miR-129-3p was found to attenuate vascular calcification, and in human, serum miR-129-3p exhibited a negative correlation with vascular calcification, suggesting that miR-129-3p could be one of the candidate predictor variables. Regression analysis demonstrated that miR-129-3p, age, dialysis duration and smoking were valid factors to establish the prediction model and nomogram for VC. The area under receiver operating characteristic curve of the model was 0.8698. The calibration curve showed that predicted probability of the model was in good agreement with actual probability and decision curve analysis indicated better net benefit of the model. Furthermore, internal validation through bootstrap process and external validation by another independent cohort confirmed the stability of the model. Conclusion: We build a diagnostic prediction model and present it as an intuitive tool based on miR-129-3p and clinical indicators to evaluate the probability of VC in hemodialysis patients, facilitating risk stratification and effective decision, which may be of great importance for reducing the risk of serious cardiovascular events.

Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways.

OBJECTIVE: Vascular calcification is a common chronic kidney disease complication. This study aimed to investigate the function of long non-coding RNA (LncRNA) H19 in vascular calcification to explore new therapeutic strategies. METHODS: We induced osteogenic differentiation and calcification of vascular smooth muscle cells (VSMCs) using ß-glycerophosphate. Then, we detected the LncRNA H19 promoter methylation status and Erk1/2 pathways using methylation-specific polymerase chain reaction and western blotting, respectively. RESULTS: Compared with the control group, high phosphorus levels induced VSMC calcification, accompanied by increases in LncRNA H19 and the osteogenic marker Runx2 and reduction of the contractile phenotype marker SM22a. LncRNA H19 knockdown inhibited osteogenic differentiation and calcification of VSMCs. However, the suppressed role of VSMC calcification caused by shRNA H19 was partially reversed by simultaneous activation of the Erk1/2 pathways. Mechanically, we found that the methylation rate of CpG islands in the LncRNA H19 promoter region was significantly lower in the high-phosphorus group, and the hypomethylation state elevated LncRNA H19 levels, which in turn regulated phosphorylated Erk1/2 expression. CONCLUSIONS: LncRNA H19 promoted osteogenic differentiation and calcification of VSMCs by regulating the Erk1/2 pathways. Additionally, hypomethylation of LncRNA H19 promoter CpG islands upregulated LncRNA H19 levels and subsequently activated Erk1/2 phosphorylation.

Effects of early recovery of renal function on adverse renal outcomes and mortality in patients with acute kidney injury: a systematic review and meta-analysis.

AIM: This study intended to scrutinize the effect of RFR time on adverse renal outcomes and mortality and try to define the cutoff of early RFR. METHODS: We conducted a literature search from database inception to February 2023. Outcome measures incorporated the progression of CKD, delivery of RRT, incidence of composite renal outcomes, and mortality. And pooled results were depicted as odds ratio (OR) and 95% confidence interval (CI). RESULTS: A total of 11 studies were finally selected (507,989 patients, mean follow-up, 3.89 years). The results exhibited that the crude mortality was lower in patients with early RFR (OR = 0.39, 95% CI: 0.16-0.95, P = 0.037). In addition, patients with early RFR had a lower incidence of progression to CKD (OR = 0.38, 95% CI: 0.17-0.85, P < 0.018), RRT (OR = 0.37, 95% CI: 0.20-0.71, P = 0.03), and composite renal outcomes (OR = 0.18, 95% CI: 0.15-0.20, P < 0.001). CKD progression-related events were significantly higher in patients whose renal function recovered after 7 days (OR = 0.69, 95% CI: 0.47-1.09, P = 0.112) than in those whose renal function recovered within 7 days (OR = 0.23, 95% CI: 0.06-0.92, P = 0.038), and the risk of RRT was lower in patients who recovered within 7 days (OR = 0.32, 95% CI: 0.15-0.66, P = 0.002) than in those who recovered after 7 days (OR = 0.72, 95% CI: 0.17-3.09, P = 0.654) or longer. CONCLUSION: Patients with early RFR had a lower risk of CKD progression, RRT, and composite renal outcomes, as well as lower crude mortality than those without early recovery, despite no marked difference in 30-day, 90-day, and 1-year mortality. We speculated that 7 days may be used as a cutoff for early RFR.

Carbon nanosol promotes plant growth and broad-spectrum resistance.

Carbon nanosol (CNS) is a carbon-based nanomaterial capable of promoting plant growth while the underlying mechanism involved in this process remains unknown. This study demonstrates that CNS promotes rice seedling growth under restricted concentrations. Macroelement transporter mutants were investigated to further investigate the CNS-mediated promotion of rice seedling growth. The genetic and physiological findings revealed that nitrate transporter 1.1B (NRT1.1B) and ammonium transporter 1 (AMT1) mutants inhibited the CNS-induced growth development of rice seedlings, whereas potassium transporter (AKT1) and phosphate transporter 8 (PT8) did not exhibit any inhibitory effects. Further investigations demonstrated the inhibition of CNS-mediated growth promotion via glutamine synthetase 1;1 (gs1;1) mutants. Additionally, the administration of CNS resulted in enhanced accumulation of chlorophyll in plants, and the promotion of CNS-induced growth was inhibited by yellow-green leaf 8 (YGL8) mutants and the chlorophyll biosynthetic gene divinyl reductase (DVR) mutants. According to these findings, the CNS promotes plant growth by stimulating chlorophyll biosynthesis. Furthermore, the presence of CNS enhanced the ability of rice to withstand blast, sheath blight (ShB), and bacterial blight. The nrt1.1b, amt1, dvr, and ygl8 mutants did not exhibit a broad spectrum effect. The positive regulation of broad-spectrum resistance in rice by GS1;1 suggests the requirement of N assimilation for CNS-mediated broad-spectrum resistance. In addition, an in vitro assay demonstrated that CNS inhibits the growth of pathogens responsible for blast, ShB, and bacterial blight, namely Magnaporthe oryzae, Rhizoctonia solani AG1-IA, and Xanthomonas oryzae pv. Oryzae, respectively. CNS application may also induce broad-spectrum resistance against bacterial and fungal pathogens, indicating that in addition to its antifungal and antibacterial properties, CNS application may also stimulate N assimilation. Collectively, the results indicate that CNS may be a potential nano-therapeutic agent for improved plant growth promotion while also providing broad-spectrum resistance.

Interaction of Sp1 and Setd8 promotes vascular smooth muscle cells apoptosis by activating Mark4 in vascular calcification.

Vascular calcification (VC) is directly related to high mortality in chronic kidney disease (CKD), and cellular apoptosis of vascular smooth muscle cells (VSMCs) is a crucial process in the initiation of VC. Microtubule affinity-regulating kinase 4 (Mark4), known as a serine/threonine protein kinase, can induce cell apoptosis and autophagy by modulating Akt phosphorylation. However, the potential functions and molecular mechanisms of Mark4 in VSMCs apoptosis and calcification need to be further explored. Initially, our data indicated that the mRNA expression of Mark4 was prominently elevated in high phosphorus-stimulated human VSMCs compared with the other members in Marks. Consistently, Mark4 expression was found to be significantly increased in the calcified arteries of both CKD patients and rats. In vitro, silencing Mark4 suppressed apoptosis-specific marker expression by promoting Akt phosphorylation, finally attenuating VSMCs calcification induced by high phosphate. Mechanically, the transcription factor Sp1 was enriched in the Mark4 promoter region and modulated Mark4 transcription. Moreover, SET domain-containing protein 8 (Setd8) was proved to interact with Sp1 and jointly participated in the transcriptional regulation of Mark4. Finally, rescue experiments revealed that Setd8 contributed to VSMCs apoptosis and calcification by modulating Mark4 expression. In conclusion, these findings reveal that Mark4 is transcriptionally activated by Sp1, which is interacted with Setd8, to promote VSMCs calcification through Akt-mediated antiapoptotic effects, suggesting that Mark4 represents a potent and promising therapeutic target for VC in CKD.

Genome-wide identification of the N6-methyladenosine regulatory genes reveals NtFIP37B increases drought resistance of tobacco (Nicotiana tabacum L.).

BACKGROUND: N6-methyladenosine (m6A) is one of the common internal RNA modifications found in eukaryotes. The m6A modification can regulate various biological processes in organisms through the modulation of alternative splicing, alternative polyadenylation, folding, translation, localization, transport, and decay of multiple types of RNA, without altering the nucleotide sequence. The three components involved in m6A modification, namely writer, eraser, and reader, mediate the abundance of RNA m6A modification through complex collaborative actions. Currently, research on m6A regulatory genes in plants is still in its infancy. RESULTS: In this study, we identified 52 candidate m6A regulatory genes in common tobacco (Nicotiana tabacum L.). Gene structure, conserved domains, and motif analysis showed structural and functional diversity among different subgroups of tobacco m6A regulatory genes. The amplification of m6A regulatory genes were mainly driven by polyploidization and dispersed duplication, and duplicated genes evolved through purified selection. Based on the potential regulatory network and expression pattern analysis of m6A regulatory genes, a significant number of m6A regulatory genes might play important roles in growth, development, and stress response processes. Furthermore, we have confirmed the critical role of NtFIP37B, an m6A writer gene in tobacco, in enhancing drought resistance. CONCLUSIONS: This study provides useful information for better understanding the evolution of m6A regulatory genes and the role of m6A modification in tobacco stress response, and lays the foundation for further elucidating the function of m6A regulatory genes in tobacco.

Genome-wide identification and analysis of WD40 proteins reveal that NtTTG1 enhances drought tolerance in tobacco (Nicotiana tabacum).

BACKGROUND: WD40 proteins, which are highly prevalent in eukaryotes, play important roles in plant development and stress responses. However, systematic identification and exploration of WD40 proteins in tobacco have not yet been conducted. RESULTS: In this study, a total of 399 WD40 regulatory genes were identified in common tobacco (Nicotiana tabacum). Gene structure and motif analysis revealed structural and functional diversity among different clades of tobacco WD40 regulatory genes. The expansion of tobacco WD40 regulatory genes was mainly driven by segmental duplication and purifying selection. A potential regulatory network of NtWD40s suggested that NtWD40s might be regulated by miRNAs and transcription factors in various biological processes. Expression pattern analysis via transcriptome analysis and qRT-PCR revealed that many NtWD40s exhibited tissue-specific expression patterns and might be involved in various biotic and abiotic stresses. Furthermore, we have validated the critical role of NtTTG1, which was located in the nuclei of trichome cells, in enhancing the drought tolerance of tobacco plants. CONCLUSIONS: Our study provides comprehensive information to better understand the evolution of WD40 regulatory genes and their roles in different stress responses in tobacco.

Impact on hospitalization and infection patterns of advanced lung cancer with lower respiratory tract infections: Targeted therapy vs. chemoradiotherapy.

Lung cancer is a prevalent and highly lethal disease often complicated by lower respiratory tract infections. Microbial patterns in these infections vary based on treatment modalities. The present study explored the impact of lung cancer treatments on pathogens and clinical characteristics in the presence of lower respiratory tract infections to inform antimicrobial drug selection. A retrospective analysis was performed that included data from 93 patients diagnosed with advanced lung cancer and lower respiratory tract infections between January 2019 and December 2021. Patients were divided into the targeted therapy and chemoradiotherapy groups. Clinical, nutritional, biochemical, infection and pathogenetic indicators were compared. Of the 93 cases, 24 were in the targeted therapy group and 69 were in the chemoradiotherapy group. Pathological type and hospitalization duration differed significantly (P<0.05), but age, sex, smoking history, alcohol consumption and underlying diseases did not (P>0.05). Lymphocyte counts differed (P<0.05), while body mass index, albumin, hemoglobin, alanine aminotransferase and creatinine levels, erythrocyte sedimentation rate, hypersensitive C-reactive protein and procalcitonin levels, and the percentage of neutrophils did not (P>0.05). Pathogenetic testing was negative in 15 patients and positive in 78 patients, with Gram-negative bacteria (61.77%), fungi (17.65%) and viruses (11.76%) predominant in the targeted therapy group. In the chemoradiotherapy group, Gram-negative bacteria (47.46%), fungi (28.81%) and viruses (16.95%) were also more prevalent. Candida albicans was the most frequent fungal infection in both groups, and mixed infections were common (50% in targeted therapy and 73.92% in chemoradiotherapy). The chemoradiotherapy group had significantly more mixed infections (P<0.05). Overall, common pathogens in both groups included Gram-negative bacteria, fungi and viruses. Chemoradiotherapy patients experienced longer hospital stays and a higher incidence of mixed infections, predominantly involving Gram-negative bacteria and fungi. The results provide valuable insights into the rational selection of empirical antibiotics and antifungals for critically ill patients with lung cancer and lower respiratory tract infections in targeted therapy or chemoradiotherapy.

Efficacy and safety of bipolar fractional radiofrequency vs. 2940-nm Er:YAG ablative fractional laser in striae distensae treatment: A split abdomen study.

BACKGROUND: Striae distensae (SD) is a challenging cosmetic condition. Ablative fractional laser (AFL) is an effective method for treating SD. Recently, fractional radiofrequency (FRF) has been shown to be a promising treatment for SD; however, few studies have shown the differences between FRF and AFL in the treatment of SD. AIMS: This study aimed to evaluate and compare the clinical efficacy and safety of bipolar FRF with 2940-nm erbium yttrium aluminum garnet (Er:YAG) AFL in the treatment of SD. PATIENTS/METHODS: Twenty volunteers with abdominal SD were enrolled in this study. One half of the abdomen was treated with 2940-nm Er:YAG AFL, whereas the other half was treated with bipolar FRF, with three sessions at 4-week intervals. Photographic evaluations of clinical improvement were conducted by two independent investigators before and after treatment, and the patients provided self-assessments. Two participants underwent three punch biopsies, one before treatment and two obtained from bilateral representative skin lesions on the abdomen 3 months following the final treatment. RESULTS: Clinical improvements were observed in SD on both sides of the abdomen after the two treatments. Post-treatment skin biopsies revealed increased thickness in the epidermis and dermis, and higher collagen and elastin density compared to those at the baseline. No statistically significant differences were observed in the clinical outcomes between the two treatment approaches. CONCLUSIONS: The efficacy and safety of bipolar FRF treatment are comparable to those of 2940-nm Er:YAG AFL treatment, providing an alternative and effective treatment for SD.

Comparative efficacy of sodium thiosulfate, bisphosphonates, and cinacalcet for the treatment of vascular calcification in patients with haemodialysis: a systematic review and network meta-analysis.

BACKGROUND: Up to now, there is no unequivocal intervention to mitigate vascular calcification (VC) in patients with hemodialysis. This network meta-analysis aimed to systematically evaluate the clinical efficacy of sodium thiosulfate, bisphosphonates, and cinacalcet in treating vascular calcification. METHODS: A comprehensive study search was performed using PubMed, Web of Science, the Cochrane Library, EMBASE and China National Knowledge Internet (CNKI) to collect randomized controlled trials (RCTs) of sodium thiosulfate, bisphosphonates, and cinacalcet for vascular calcification among hemodialysis patients. Then, network meta-analysis was conducted using Stata 17.0 software. RESULTS: In total, eleven RCTs including 1083 patients were qualified for this meta-analysis. We found that cinacalcet (SMD - 0.59; 95% CI [-0.95, -0.24]) had significant benefit on vascular calcification compared with conventional therapy, while sodium thiosulfate or bisphosphonates did not show such efficiency. Furthermore, as for ranking the efficacy assessment, cinacalcet possessed the highest surface under the cumulative ranking curve (SUCRA) value (88.5%) of lessening vascular calcification and was superior to sodium thiosulfate (50.4%) and bisphosphonates (55.4%). Thus, above results suggested that cinacalcet might be the most promising drug for vascular calcification treatment in hemodialysis patients. Mechanistically, our findings illustrated that cinacalcet reduced serum calcium (SMD - 1.20; 95% CI [-2.08, - 0.33]) and showed the tendency in maintaining the balance of intact Parathyroid Hormone (iPTH) level. CONCLUSIONS: This network meta-analysis indicated that cinacalcet appear to be more effective than sodium thiosulfate and bisphosphonates in mitigating vascular calcification through decreasing serum calcium and iPTH. And cinacalcet might be a reasonable option for hemodialysis patients with VC in clinical practice. SYSTEMATIC REVIEW REGISTRATION: [ http://www.crd.york.ac.uk/PROSPERO ], identifier [CRD42022379965].

The efficacy and safety of sacubitril/valsartan in chronic kidney disease: a systematic review and meta-analysis.

BACKGROUND: Sacubitril/valsartan, a new pharmacological class of angiotensin receptor neprilysin inhibitor, is beneficial to heart failure through blocking the degradation of natriuretic peptides and inhibiting renin-angiotensin-aldosterone system (RAAS) activation which also relate to the pathophysiologic mechanisms of chronic kidney disease (CKD). However, its effects on CKD remain unclear. To assess the efficacy and safety of sacubitril/valsartan for patients with CKD, we performed this meta-analysis. METHODS: The Embase, PubMed and the Cochrane Library were searched for randomized controlled trials (RCTs) that compared sacubitril/valsartan with ACEI/ARBs in patients with CKD whose estimated glomerular filtration rate (eGFR) was below 60 mL/min/1.73 m2. We adopted the Cochrane Collaboration tool for assessing the risk of bias. The effect size was estimated using the odds ratio (OR) with 95% confidence interval (CI). RESULTS: Six trials with a total of 6217 patients with CKD were included. In terms of cardiovascular events, sacubitril/valsartan attenuated the risk of cardiovascular death or heart failure hospitalization (OR: 0.68, 95% CI 0.61-0.76, P < 0.00001, I2 = 43%). With respect to renal function, sacubitril/valsartan prevented the incidence of serum creatinine (Scr) elevation among patients with CKD (OR: 0.79, 95% CI 0.67-0.95, P = 0.01, I2 = 0%). Subgroup analysis about eGFR demonstrated that with long follow-up, sacubitril/valsartan significantly decreased the number of patients with more than 50% reduction in eGFR compared with ACEI/ARBs (OR: 0.52, 95% CI 0.32-0.84, P = 0.008, I2 = 9%). In patients with CKD, the incidence of end-stage renal disease (ESRD) was reduced with sacubitril/valsartan treatment, despite no statistically significant difference between the two groups (OR: 0.59, 95% CI 0.29-1.20, P = 0.14, I2 = 0%). As for the safety, we found that sacubitril/valsartan was associated with the occurrence of hypotension (OR: 1.71, 95% CI 1.15-2.56, P = 0.008, I2 = 51%). However, there was no trend towards increasing the risk of hyperkalemia in patients who received sacubitril/valsartan (OR: 1.09, 95% CI 0.75-1.60, P = 0.64, I2 = 64%). CONCLUSION: This meta-analysis indicated that sacubitril/valsartan improved renal function and conferred effective cardiovascular benefits in patients with CKD, without serious safety issues being observed. Thus, sacubitril/valsartan may be a promising option for patients with CKD. Certainly, further large-scale randomized controlled trials are needed to confirm these conclusions. SYSTEMATIC REVIEW REGISTRATION: [ https://inplasy.com/inplasy-2022-4-0045/ ], identifier [INPLASY202240045].

The association of hemoglobin ethylene oxide levels with albuminuria in US adults: analysis of NHANES 2013-2016.

Ethylene oxide (EO) is a common chemical contaminant in the environment and associated with the occurrence of multiple clinical diseases. This study aimed to explore the association of hemoglobin ethylene oxide (HbEO) levels with the risk of albuminuria in a representative sample of US adults. In total, 3523 participants from National Health and Nutrition Examination Survey (NHANES) 2013-2016 were enrolled and classified into four groups based on HbEO. Restricted cubic spline plots and multiple logistic regression were performed to investigate the connection between HbEO levels and albuminuria, and mediation analysis was applied to elucidate the potential mechanism for the effect of HbEO concentrations on albuminuria. In the results, compared with the extreme quartile of HbEO levels, the weighted prevalence of albuminuria was significantly increased in participants with highest quartile (Q4 vs Q1, 11.2% vs 8.1%). Restricted cubic spline plots revealed that the risk of albuminuria raised non-linearly and positively with elevated HbEO level. After adjusting for confounders, the logistic regression suggested that the risk of albuminuria was enhanced by 12% for each one-unit increase in log-2-transformed HbEO (OR = 1.12, 95% CI, 1.03-1.22, P = 0.007). Moreover, the multivariate ORs (95% CIs) on albuminuria was increased across the increasing HbEO quartiles (Q4 vs Q1, OR = 1.54, 95% CI, 1.09-2.17; P for trend = 0.029). Furthermore, the impact of high HbEO level on albuminuria was partially related to inflammation markers, including white blood cells (17.2%), neutrophils (22.1%), and lymphocytes (19.5%). To sum up, our study identified that high HbEO levels increased the risk of albuminuria in representative population of US adults, and several inflammatory mediators might be potentially involved in EO-associated albuminuria.

Carbon nanosol-induced assemblage of a plant-beneficial microbiome consortium.

Carbon nanosol (CNS) is a carbon-based nanomaterial that promotes plant growth; however, its functional mechanisms and effects on the microbiome are not fully understood. Here, we explored the effects of CNS on the relationship between the soil, endophytic microbiomes and plant productivity. CNS treatment increased the fresh biomass of tobacco (Nicotiana tabacum L.) plants by 27.4% ± 9.9%. Amplicon sequencing analysis showed that the CNS treatment significantly affected the composition and diversity of the microbial communities in multiple ecological niches associated with tobacco, especially the bulk soil and stem endophytic microbiome. Furthermore, the application of CNS resulted in enhanced network connectivity and stability of the microbial communities in different niches, particularly in the soil, implying a strengthening of certain microbial interactions. Certain potentially growth-promoting root endophytic bacteria were more abundant under the CNS treatment. In addition, CNS increased the abundance of some endophytic microbial functional genes known to enhance plant growth, such as those associated with nutrient metabolism and the plant hormone biosynthesis pathways. We isolated two bacterial strains (Sphingopyxis sp. and Novosphingobium sp.) that were enriched under CNS treatment, and they were confirmed to promote tobacco plant growth in vitro. These results suggested that CNS might, at least in part, promote plant growth by enriching beneficial bacteria in the microbiome.

Boron Bifunctional Catalysts for Rapid Degradation of Persistent Organic Pollutants in a Metal-Free Electro-Fenton Process: O2 and H2O2 Activation Process.

Metals usually served as the active sites of the heterogeneous bifunctional electro-Fenton reaction, which faced the challenge of poor stability under acidic or even neutral conditions. Exploring a metal-free heterogeneous bifunctional electro-Fenton catalyst can effectively solve the above problems. In this work, a stable metal-free heterogeneous bifunctional boron-modified porous carbon catalyst (BTA-1000) was synthesized. For the BTA-1000 catalyst, the yield of H2O2 (294 mg/L) significantly increased. The degradation rate of phenol by BTA-1000 (0.242 min-1) increased by an order of magnitude, compared with the porous carbon catalyst (0.0105 min-1). The BTA catalyst could rapidly degrade industrial dye wastewater, and its specific energy consumption was 5.52 kW h kg-1 COD-1, lower than that in previous reports (6.38-7.4 kW h kg-1 COD-1). DFT and XPS revealed that C═O and -BC2O groups jointly promoted the generation of H2O2, and the -BCO2 group played dominant roles in the generation of •OH because the oxygen atom near the electron-giving groups (-BCO2 group) facilitated the formation of hydrogen bond and H2O2 adsorption. This work gained deep insights into the reaction mechanism of the boron-modified porous carbon catalyst, which helped to guide the development of metal-free heterogeneous bifunctional electro-Fenton catalysts.

Effect of cardiac function in patients with gastrointestinal cancer with or without acute kidney injury assessed using a non-invasive impedance cardiography: a case-control study.

OBJECTIVES: This study aimed to analyze the possible causes of changes in cardiac function and investigate the feasibility of clinical assessment of gastrointestinal cancer in patients with or without acute kidney injury (AKI) assessed using a non-invasive impedance cardiography (ICG, Bioz. Cardio Dynamics, USA) to identify independent risk factors. METHODS: Patients admitted to the Fourth Hospital of Hebei Medical University, China, between May 1, 2019, and February 15, 2022, were included in this study. A total of 51 patients with gastrointestinal cancer (31 men and 20 women, mean age 61.1 ± 10.9 years) with or without AKI were evaluated for ICG. A total of 19 patients underwent ultrasound cardiography (UCG) and ICG evaluations. RESULT: There was a significant positive correlation between cardiac output (CO), cardiac index (CI), stroke volume (SV), left cardiac work index (LCWI), and ejection fraction (EF) measured using UCG and ICG. The relationship was observed between COICG and COUCG (r = 0.707, P = 0.001), CIICG and CIUCG (r = 0.718, P = 0.001), SVICG and SVUCG (r = 0.837, P < 0.001), and LCWIICG and EFUCG (r = 0.540, P = 0.017). Cardiac function parameters measured using ICG were statistically different between patients with gastrointestinal cancer with or without AKI (P ≤ 0.05). Multivariate analysis revealed that AKI independently affects cardiac function in patients with gastrointestinal cancer. CONCLUSIONS: UCG and ICG methods are significantly associated with cardiac function in patients with or without AKI, and patients with gastrointestinal cancer with AKI are worse than those without AKI. AKI is an independent risk factor for cardiac function in patients with gastrointestinal cancer.

High-throughput creation of Nicotiana tabacum gene-targeted mutants based on CRISPR/Cas9.

KEY MESSAGE: 4382 available sgRNAs targeting 1060 tobacco genes were obtained, and 10,682 targeted mutants were created using high-throughput methods. Four optimization experiments were established to solve problems encountered during genetic transformation.

Deciphering plant cell-cell communications using single-cell omics data.

Plants have various cell types that respond to different environmental factors, and cell-cell communication is the fundamental process that controls these plant responses. The emergence of single-cell techniques provides opportunities to explore features unique to each cell type and construct a comprehensive cell-cell communication (CCC) network. Although the most current successes of CCC inference were achieved in animal research, computational methods can also be directly applied to plants. This review describes the current major models for cell-cell communication inference and summarizes the computational tools based on single-cell omics datasets. In addition, we discuss the limitations of plant cell-cell communication research and propose new directions to expand the field in meaningful ways.