Fast Interfacial Defluorination Kinetics Enables Stable Cycling of Low-Temperature Lithium Metal Batteries.

The development of low-temperature lithium metal batteries (LMBs) encounters significant challenges because of severe dendritic lithium growth during the charging/discharging processes. To date, the precise origin of lithium dendrite formation still remains elusive due to the intricate interplay between the highly reactive lithium metal anode and organic electrolytes. Herein, we unveil the critical role of interfacial defluorination kinetics of localized high-concentration electrolytes (LHCEs) in regulating lithium dendrite formation, thereby determining the performance of low-temperature LMBs. We investigate the impact of solvation structures of LHCEs on low-temperature LMBs by employing tetrahydrofuran (THF) and 2-methyltetrahydrofuran (2-MeTHF) as comparative solvents. The combination of comprehensive characterizations and theoretical simulations reveals that the THF-based LHCE featured with a strong solvation strength exhibits fast interfacial defluorination reaction kinetics, thus leading to the formation of an amorphous and inorganic-rich solid-electrolyte interphase (SEI) that can effectively suppress the growth of lithium dendrites. As a result, the highly reversible Li metal anode achieves an exceptional Coulombic efficiency (CE) of up to ∼99.63% at a low temperature of -30 °C, thereby enabling stable cycling of low-temperature LMB full cells. These findings underscore the crucial role of electrolyte interfacial reaction kinetics in shaping SEI formation and provide valuable insights into the fundamental understanding of electrolyte chemistry in LMBs.

Progress and Perspectives on the Development of Pouch-Type Lithium Metal Batteries.

Lithium (Li) metal batteries (LMBs) are the "holy grail" in the energy storage field due to their high energy density (theoretically >500 Wh kg-1 ). Recently, tremendous efforts have been made to promote the research & development (R&D) of pouch-type LMBs toward practical application. This article aims to provide a comprehensive and in-depth review of recent progress on pouch-type LMBs from full cell aspect, and to offer insights to guide its future development. It will review pouch-type LMBs using both liquid and solid-state electrolytes, and cover topics related to both Li and cathode (including LiNix Coy Mn1-x-y O2 , S and O2 ) as both electrodes impact the battery performance. The key performance criteria of pouch-type LMBs and their relationship in between are introduced first, then the major challenges facing the development of pouch-type LMBs are discussed in detail, especially those severely aggravated in pouch cells compared with coin cells. Subsequently, the recent progress on mechanistic understandings of the degradation of pouch-type LMBs is summarized, followed with the practical strategies that have been utilized to address these issues and to improve the key performance criteria of pouch-type LMBs. In the end, it provides perspectives on advancing the R&Ds of pouch-type LMBs towards their application in practice.

Combination of smoking and Epstein-Barr virus DNA is a predictor of poor prognosis for nasopharyngeal carcinoma: a long-term follow-up retrospective study.

BACKGROUND: This retrospective study was performed to determine the prognostic potential of smoking and its combination with pre-treatment plasma Epstein-Barr virus (EBV) DNA levels in patients with nasopharyngeal carcinoma (NPC). METHODS: Medical records of 1080 non-metastatic NPC patients who received intensity-modulated radiotherapy were reviewed. Male patients were categorized as never and ever smokers, and the smoking amount, duration, and cumulative consumption were used to evaluate dose-dependent effects. Survival outcomes were assessed using Kaplan-Meier survival analysis and the multivariate Cox regression analysis. Propensity score matching (PSM) was constructed. RESULTS: The 5-year overall survival (OS) was worse for ever smokers than never smokers, and significantly decreased with the increase of smoking amount, duration, and cumulative consumption. Compared with never smokers, the multivariate-adjusted hazard ratio (HR) of death was higher in ever smokers (HR = 1.361, P = 0.049), those smoked ≥20 cigarettes/day (HR = 1.473, P = 0.017), those smoked for ≥30 years (HR = 1.523, P = 0.023), and those cumulative smoked for ≥30 pack-years (HR = 1.649, P = 0.005). The poor prognostic effects of smoking was also confirmed in the PSM analysis. The combination of cumulative smoking consumption and pre-treatment EBV DNA levels was proven to be an independent poor prognostic factor for male NPC, and the risk of death, progression, and distant metastases gradually increased with both factors (P < 0.001). CONCLUSIONS: Combination of smoking and pre-treatment EBV DNA levels as a predictor of poor prognosis could further improve the risk stratification and prognostication for NPC.

Use of latent profile analysis and k-means clustering to identify student anxiety profiles.

BACKGROUND: Anxiety disorders are often the first presentation of psychopathology in youth and are considered the most common psychiatric disorders in children and adolescents. This study aimed to identify distinct student anxiety profiles to develop targeted interventions. METHODS: A cross-sectional study was conducted with 9738 students in Yingshan County. Background characteristics were collected and Mental Health Test (MHT) were completed. Latent profile analysis (LPA) was applied to define student anxiety profiles, and then the analysis was repeated using k-means clustering. RESULTS: LPA yielded 3 profiles: the low-risk, mild-risk and high-risk groups, which comprised 29.5, 38.1 and 32.4% of the sample, respectively. Repeating the analysis using k-means clustering resulted in similar groupings. Most students in a particular k-means cluster were primarily in a single LPA-derived student profile. The multinomial ordinal logistic regression results showed that the high-risk group was more likely to be female, junior, and introverted, to live in a town, to have lower or average academic performance, to have heavy or average academic pressure, and to be in schools that have never or occasionally have organized mental health education activities. CONCLUSIONS: The findings suggest that students with anxiety symptoms may be categorized into distinct profiles that are amenable to varying strategies for coordinated interventions.

Isolation and genomic analysis of temperate phage 5W targeting multidrug-resistant Acinetobacter baumannii.

Temperate phages are potential therapeutic agents, but only a few temperate phages infecting multidrug-resistant Acinetobacter baumannii have been identified. In this study, we isolated 5W, a temperate phage that infects multidrug-resistant A. baumannii, from pond water using the enrichment method. A member of the Siphoviridae family, 5W has a narrow host range and infected only four of 19 A. baumannii clinical isolates. It exhibited rapid adsorption (> 90% in 6 min), a latency period of 20 min, and a burst size of ~ 180 plaque-forming units (PFU/cell). 5W contains a linear double-stranded DNA (dsDNA) genome of 43,032 bp with a GC content of 39.85%. The 5W genome contains 61 open reading frames, including lysogen-forming genes, but lacks any known virulence and antibiotic resistance genes. The lysin of 5W is an N-acetyl-ß-D-muramidase belonging to the GH_108 family. The α-helical structure and highly positively charged amino acids in the C-terminal region indicate potential antibacterial activity against A. baumannii, and the M/S subunits of the restriction endonuclease are inserted into the lysogenic gene cluster. Comparative genome analysis revealed high similarity with two different prophages in A. baumannii ABCR01, suggesting that 5W may be derived from recombination of other prophages.

EZH2-mediated repression of Dkk1 promotes hepatic stellate cell activation and hepatic fibrosis.

EZH2, a histone H3 lysine-27-specific methyltransferase, is involved in diverse physiological and pathological processes including cell proliferation and differentiation. However, the role of EZH2 in liver fibrosis is largely unknown. In this study, it was identified that EZH2 promoted Wnt pathway-stimulated fibroblasts in vitro and in vivo by repressing Dkk-1, which is a Wnt pathway antagonist. The expression of EZH2 was increased in CCl4 -induced rat liver and primary HSCs as well as TGF-ß1-treated HSC-T6, whereas the expression of Dkk1 was reduced. Silencing of EZH2 prevented TGF-ß1-induced proliferation of HSC-T6 cells and the expression of α-SMA. In addition, knockdown of Dkk1 promoted TGF-ß1-induced activation of HSCs. Moreover, silencing of EZH2 could restore the repression of Dkk-1 through trimethylation of H3K27me3 in TGF-ß1-treated HSC-T6 cells. Interestingly, inhibition of EZH2 had almost no effect on the activation of HSC when Dkk1 was silenced. Collectively, EZH2-mediated repression of Dkk1 promotes the activation of Wnt/ß-catenin pathway, which is an essential event for HSC activation.

Methylation of Septin9 mediated by DNMT3a enhances hepatic stellate cells activation and liver fibrogenesis.

Liver fibrosis, resulting from chronic and persistent injury to the liver, is a worldwide health problem. Advanced liver fibrosis results in cirrhosis, liver failure and even hepatocellular cancer (HCC), often eventually requiring liver transplantation, poses a huge health burden on the global community. However, the specific pathogenesis of liver fibrosis remains not fully understood. Numerous basic and clinical studies have provided evidence that epigenetic modifications, especially DNA methylation, might contribute to the activation of hepatic stellate cells (HSCs), the pivotal cell type responsible for the fibrous scar in liver. Here, reduced representation bisulfite sequencing (RRBS) and bisulfite pyrosequencing PCR (BSP) analysis identified hypermethylation status of Septin9 (Sept9) gene in liver fibrogenesis. Sept9 protein was dramatically decreased in livers of CCl4-treated mice and immortalized HSC-T6 cells exposed to TGF-ß1. Nevertheless, the suppression of Sept9 could be blocked by DNMT3a-siRNA and DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5-azadC). Overexpressed Sept9 attenuated TGF-ß1-induced expression of myofibroblast markers α-SMA and Col1a1, accompanied by up-regulation of cell apoptosis-related proteins. Conversely, RNAi-mediated silencing of Sept9 enhanced accumulation of extracellular matrix. These observations suggested that Sept9 contributed to alleviate liver fibrosis might partially through promoting activated HSCs apoptosis and this anti-fibrogenesis effect might be blocked by DNMT-3a mediated methylation of Sept9. Therefore, pharmacological agents that inhibit Sept9 methylation and increase its expression could be considered as valuable treatments for liver fibrosis.

HMGA2, a driver of inflammation, is associated with hypermethylation in acute liver injury.

Acute liver injury (ALI) is characteristic of abrupt hepatic dysfunction and inflammatory response. Activaion of Kupffer cells (KCs) plays a central role in the pathogenesis of ALI. Since the High Mobility Group A protein2 (HMGA2) occurs as a driver at critical stage of hepatocellular carcinoma, herein, we investigated the role of HMGA2 in macrophage activation during ALI. Our study found that the expression of HMGA2 decreased dramatically both in KCs isolated from the liver in mice with ALI and in LPS-induced RAW264.7 cell lines. Moreover, loss- and gain-of-function studies suggested that HMGA2 could enhance the expression of pro-inflammatory cytokines including TNF-α, IL-6 and IL-1ß. These results indicated that HMGA2 may play an essential role in macrophage activation during ALI. Additionally, our results showed the expression of HMGA2 was up-regulated when LPS-induced RAW264.7 cells were treated with 5-aza-2-deoxycytidine. Furthermore, silencing of DNMT1, DNMT3a, DNMT3b could respectively prevent the down-expression of HMGA2 in LPS-induced RAW264.7 cells. In conclusion, HMGA2 promotes the release of pro-inflammatory cytokines through NF-κB pathway, and the dysregulation of HMGA2 may involve with hypermethylation.

Glutamine reduces myocardial cell apoptosis in a rat model of sepsis by promoting expression of heat shock protein 90.

BACKGROUND: Myocardial cell injury and cardiac myocyte apoptosis are associated with sepsis. Glutamine (Gln) has been reported to repair myocardial cell injury. The aim of this study was to explore the role of Gln on cardiac myocytes in a cecal ligation and puncture (CLP) model of sepsis in Wistar rats. MATERIALS AND METHODS: Following induction of sepsis in a CLP rat model, viral encoding heat shock protein 90 (Hsp90) gene and Hsp90dsDNA were designed to express and knockdown Hsp90, respectively. Rat cardiac tissues were examined histologically, and apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, Hsp90, p53 upregulated modulator of apoptosis, and p53 was measured by western blotting and real-time polymerase chain reaction. Caspase-3, caspase-8, and caspase-9 were detected by enzyme-linked immunosorbent assay. RESULTS: Rat cardiac myocyte damage induced by CLP was reduced by Gln treatment and Hsp90 overexpression, and these changes were reversed by Hsp90 knockdown. Bcl-2 expression, Bcl-2-associated X protein, p53, p53 upregulated modulator of apoptosis, caspase-8, caspase-9, and caspase-3 activities were significantly upregulated in the CLP model, which were reduced by Gln treatment and Hsp90 overexpression. CONCLUSIONS: Gln reduced apoptosis of cardiac myocytes in a rat model of sepsis, by promoting Hsp90 expression. Further studies are needed to determine the possible therapeutic action of Gln in sepsis in human tissue.

Role of NLRC5 in progression and reversal of hepatic fibrosis.

BACKGROUND: NLRC5, as the largest member of NLRs family, has recently been identified as a critical regulator of immune responses through negatively regulating NF-κB which is associated with the development of hepatic fibrosis. However, the expression and potential roles of NLRC5 in hepatic fibrosis and its reversal are still to be defined. METHODS: C57BL/6 mice were treatment with carbon tetrachloride (CCl4) induce hepatic fibrosis and its reversal. In vitro, models of hepatic fibrosis and its reversal are established by the treatment with TGF-ß and MDI. The expression of NLRC5 was determined by RT-PCR, Western blot and immunohistochemistry. Consequently, NLRC5 was overexpressed or knockdown by transfecting PEGFP-C2-NLRC5 or NLRC5-siRNA respectively in the reversal of hepatic fibrosis, and the expression of fibrogenic genes such as α-SMA and Col1α1 was quantified. The NF-κB activity was detected as well. RESULTS: Immunohistochemistry, RT-PCR and Western blot analysis with liver tissues and primary HSCs showed that NLRC5 was highly expressed in hepatic fibrosis and correspondingly decreased in the reversal stage. The differential expression of NLRC5 was confirmed in vitro. Enforced NLRC5 expression increased the expression of α-SMA and Col1α1, and blockade of NLRC5 reduced the fibrotic response. While the opposite expression of phosphorylated NF-кB p65 and phospho-IκBα was found. CONCLUSION: NLRC5 is differentially expressed in hepatic tissues and hepatic stellate cells during hepatic fibrosis and its reversal. All the data indicated that NLRC5 may play a crucial role in regulating the reversal of hepatic fibrosis through NF-κB signaling pathway.

PTP1B confers liver fibrosis by regulating the activation of hepatic stellate cells.

Liver fibrosis is a reversible wound-healing response to chronic hepatic injuries. Activation of hepatic stellate cells (HSCs) plays a pivotal role in the development of hepatic fibrosis. The currently accepted mechanism for the resolution of liver fibrosis is the apoptosis and inactivation of activated HSCs. Protein tyrosine phosphatase 1B (PTP1B), a prototype of non-receptor protein tyrosine phosphatase, is proved to be a vital modulator in cardiac fibrogenesis. However, the precise role of PTP1B on liver fibrosis and HSC activation is still unclear. Our study showed that the expression of PTP1B was elevated in fibrotic liver but reduced after spontaneous recovery. Moreover, stimulation of HSC-T6 cells with transforming growth factor-ß1 (TGF-ß1) resulted in a dose/time-dependent increase of PTP1B mRNA and protein. Co-incubation of HSC-T6 cells with PTP1B-siRNA inhibited the cell proliferation and activation induced by TGF-ß1. Additionally, both mRNA and protein of PTP1B were dramatically decreased in inactivated HSCs after treated with adipogenic differentiation mixture (MDI). Over-expression of PTP1B hindered the inactivation of HSC-T6 cells induced by MDI. These observations revealed a regulatory role of PTP1B in liver fibrosis and implied PTP1B as a potential therapeutic target.

Role of histone deacetylases(HDACs) in progression and reversal of liver fibrosis.

Liver fibrosis refers to a reversible wound healing process response to chronic liver injuries. Activation of hepatic stellate cells (HSCs) is closely correlated with the development of liver fibrosis. Histone deacetylases(HDACs) determine the acetylation levels of core histones to modulate expression of genes. To demonstrate the link between HDACs and liver fibrosis, CCl4-induced mouse liver fibrosis model and its spontaneous reversal model were established. Results of the current study demonstrated that deregulation of liver HDACs may involved in the development of liver fibrosis. Among 11 HDACs tested in our study (Class I, II, and IV HDACs), expression of HDAC2 was maximally increased in CCl4-induced fibrotic livers but decreased after spontaneous recovery. Moreover, expression of HDAC2 was elevated in human liver fibrotic tissues. In this regard, the potential role of HDAC2 in liver fibrosis was further evaluated. Our results showed that administration of HSC-T6 cells with transforming growth factor-beta1 (TGF-ß1) resulted in an increase of HDAC2 protein expression in dose- and time-dependent manners. Moreover, HDAC2 deficiency inhibited HSC-T6 cell proliferation and activation induced by TGF-ß1. More importantly, the present study showed HDAC2 may regulate HSCs activation by suppressing expression of Smad7, which is a negative modulator in HSCs activation and liver fibrosis. Collectively, these observations revealed that HDAC2 may play a pivotal role in HSCs activation and liver fibrosis while deregulation of HDACs may serve as a novel mechanism underlying liver fibrosis.

The curative effect analysis and nursing measures of the transvaginal myomectomy and transabdominal myomectomy.

To analyze the curative effects of the transvaginal myomectomy (TVM) and the traditional transabdominal myomectomy (TAM). The group with traditional TAM received routine preoperative nursing guidance and postoperative care. While the group with TVM received preoperative strengthened psychological care, vaginal preparation and postoperative strengthened vagina nursing, paying attention to the prevention and treatment of complications, and maintaining effective pelvic draining and other nursing measures. After that, the statistical processing and analysis were used to compared the intraoperative blood loss, operating time, postoperative infusion time, hospitalization time, postoperative eating, postoperative ambulation, the usage rate of postoperative analgesic, postoperative morbidity and postoperative complications between the two groups Comparison between TVM group and TAM group showed that the difference of the operating time, postoperative infusion time, hospitalization time, postoperative eating, postoperative ambulation, the usage rate of postoperative analgesic, postoperative morbidity and postoperative complications between the two groups were statistically significant (P<0.05). While the difference of intraoperative blood loss between the two groups were not statistically significant (P>0.05). The operating time in TVM group was shorter than TAM group; the postoperative eating, postoperative ambulation were earlier than the TAM group; the duration of postoperative transfusion and hospitalization in TVM were shorter than the TVM group; and the usage rate of postoperative analgesic and postoperative morbidity and complications in TVM group were less than the TAM group. TVM have the advantages of minimal invasion, quick recovery, less pain, shorter hospitalization duration and notable curative effect etc. Strengthening nursing care is the key to the success of treatment.

Online interpretable dynamic prediction models for clinically significant posthepatectomy liver failure based on machine learning algorithms: A retrospective cohort study.

BACKGROUND: Posthepatectomy liver failure (PHLF) is the leading cause of mortality in patients undergoing hepatectomy. However, practical models for accurately predicting the risk of PHLF are lacking. This study aimed to develop precise prediction models for clinically significant PHLF. METHODS: A total of 226 patients undergoing hepatectomy at a single center were recruited. The study outcome was clinically significant PHLF. Five pre- and postoperative machine learning (ML) models were developed and compared with four clinical scores, namely, the MELD, FIB-4, ALBI, and APRI scores. The robustness of the developed ML models was internally validated using 5-fold cross-validation by calculating the average of the evaluation metrics and was externally validated on an independent temporal dataset, including the area under the curve (AUC) and the area under the precision‒recall curve (AUPRC). SHapley Additive exPlanations analysis was performed to interpret the best performance model. RESULTS: Clinically significant PHLF was observed in 23 of 226 patients (10.2%). The variables in the preoperative model included creatinine, total bilirubin, and Child‒Pugh grade. In addition to the above factors, the extent of resection was also a key variable for the postoperative model. The pre- and postoperative artificial neural network (ANN) models exhibited excellent performance, with mean AUCs of 0.766 and 0.851, respectively, and mean AUPRC values of 0.441 and 0.645, whereas the MELD, FIB-4, ALBI, and APRI scores reached AUCs of 0.714, 0.498, 0.536 and 0.551, respectively, and AUPRC values of 0.204, 0.111, 0.128 and 0.163, respectively. In addition, the AUCs of the pre- and postoperative ANN models were 0.720 and 0.731, respectively, and the AUPRC values were 0.380 and 0.408, respectively, on the temporal dataset. CONCLUSION: Our online interpretable dynamic ML models outperformed common clinical scores and could function as a clinical decision support tool to identify patients at high risk of PHLF pre- and postoperatively.

Hypoxia improves self-renew and migration of urine-derived stem cells by upregulating autophagy and mitochondrial function through ERK signal pathway.

Urine-derived stem cells (USCs) are autologous stem cells with self-renewal ability and multi-lineage differentiation potential. Our previous studies have shown that hypoxia preconditioning can improve self-renewal and migration abilities of USCs by up-regulating autophagy. The purpose of this study was to investigate the specific mechanism by which hypoxia treatment promotes the biological function of USCs. We found that hypoxia treatment upregulated the expression of phosphralated ERK protein without affecting the expression of total ERK protein. Inhibiting ERK signaling with the PD98059 inhibitor decreased cell proliferation, migration and colony formation during hypoxia treatment. Hypoxia increased ATP production, mitochondrial membrane potential and mt-DNA copy number, which were reversed by inhibiting the ERK signal. Additionally, the number of autophagosomes and autophagic lysosomes was significantly lower in PD98059 group than in the hypoxia group. PD98059 treatment inhibited the up-regulation of autophagy related proteins induced by hypoxia. Therefore, this study suggests that hypoxia improves the self-renewal and migration abilities of USCs by upregulating autophagy and mitochondrial function through ERK signaling pathway. This finding may provide a new therapeutic mechanism for hypoxia pretreated USCs as a source of stem cell transplantation.

Origin of dendrite-free lithium deposition in concentrated electrolytes.

The electrolyte solvation structure and the solid-electrolyte interphase (SEI) formation are critical to dictate the morphology of lithium deposition in organic electrolytes. However, the link between the electrolyte solvation structure and SEI composition and its implications on lithium morphology evolution are poorly understood. Herein, we use a single-salt and single-solvent model electrolyte system to systematically study the correlation between the electrolyte solvation structure, SEI formation process and lithium deposition morphology. The mechanism of lithium deposition is thoroughly investigated using cryo-electron microscopy characterizations and computational simulations. It is observed that, in the high concentration electrolytes, concentrated Li+ and anion-dominated solvation structure initiate the uniform Li nucleation kinetically and favor the decomposition of anions rather than solvents, resulting in inorganic-rich amorphous SEI with high interface energy, which thermodynamically facilitates the formation of granular Li. On the contrary, solvent-dominated solvation structure in the low concentration electrolytes tends to exacerbate the solvolysis process, forming organic-rich mosaic SEI with low interface energy, which leads to aggregated whisker-like nucleation and growth. These results are helpful to tackle the long-standing question on the origin of lithium dendrite formation and guide the rational design of high-performance electrolytes for advanced lithium metal batteries.

Regulating Li2S Deposition by Ostwald Ripening in Lithium-Sulfur Batteries.

The lithium-sulfur (Li-S) batteries have attracted tremendous attention from both academia and industry for their high energy density and environmental benignity. However, the cell performance suffers from the passivation of the conductive matrix caused by uncontrolled lithium sulfide (Li2S) deposition. Therefore, regulation of Li2S deposition is essential to advanced Li-S batteries. In this work, the role of temperature in regulating Li2S deposition is comprehensively investigated. At room temperature (25 °C), Li2S exhibits a two-dimensional (2D) growth mode. The dense and insulating Li2S film covers the conductive surface rapidly, inhibiting the charge transfer for subsequent polysulfide reduction. Consequently, the severe passivation of the conductive surface degrades the cell performance. In contrast, three-dimensional (3D) Li2S is formed at a high temperature (60 °C) because of a faster Ostwald ripening rate at an elevated temperature. The passivation of the conductive matrix is mitigated effectively, and the cell performance is enhanced significantly, thanks to the formation of 3D Li2S. Ostwald ripening is also valid for Li-S cells under rigorous conditions. The cell working at 60 °C achieves a high specific capacity of 1228 mA h g-1 under the conditions of high S loading and a lean electrolyte (S loading = 3.6 mg cm-2, electrolyte/sulfur ratio = 3 µL mg-1), which is substantially higher than that at 25 °C. This work enriches the intrinsic understanding of Li2S deposition in Li-S batteries and provides facile strategies for improving the cell performance under practical conditions.

Ultrasound dynamic monitoring of IVCD to guide application of CRRT in patients with renal failure combined with acute heart failure.

We explored the application value of bedside ultrasound dynamic monitoring of the inferior vena cava diameter (IVCD) and collapse with sniff (inferior vena cava collapsibility index [IVCCI]) to guide dehydration adjustment in continuous renal replacement therapy (CRRT) in patients with combined renal failure and acute heart failure. We selected 90 patients with combined renal and acute heart failure who required CRRT in the intensive care unit (ICU) from January 2019 to June 2021. According to different blood volume assessment methods, patients were randomly divided into ultrasound, experience, and control groups. We compared serum creatinine, potassium, and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels; time to improved heart failure symptoms; CRRT time; ventilator use; ICU length of stay; vasopressor use; and incidence of adverse events among groups. There were no significant differences in serum creatinine, potassium, and NT-proBNP levels in pairwise comparisons among groups before and after CRRT (P > 0.05). The time to improved heart failure symptoms, CRRT time, and ICU length of stay in the ultrasound and experience groups were lower than those in the control group; the differences were statistically significant (P < 0.05). Ventilator use duration was lower in the ultrasound and experience groups compared with the control group, with a statistically significant difference between the ultrasound and control groups (P < 0.05). The duration of vasopressor use in the ultrasound and control groups was lower than that in the experience group; the difference was statistically significant (P < 0.05). The incidence of adverse events was lower in the ultrasound group compared with the experience and control groups; the difference was statistically significant (P < 0.05). Ultrasound dynamic monitoring of IVCD and collapse with sniff can accurately assess blood volume status, and provide guidance for dehydration adjustments in CRRT and rapid relief of heart failure symptoms in patients with combined renal and acute heart failure.

Surface Transformation Enables a Dendrite-Free Zinc-Metal Anode in Nonaqueous Electrolyte.

Significant challenges remain in developing rechargeable zinc batteries mainly because of reversibility problems on zinc-metal anodes. The dendritic growth and hydrogen evolution on zinc electrodes are major obstacles to overcome in developing practical and safe zinc batteries. Here, a dendrite-free and hydrogen-free Zn-metal anode with high Coulombic efficiency up to 99.6% over 300 cycles is realized in a newly designed nonaqueous electrolyte, which comprises an inexpensive zinc salt, zinc acetate, and a green low-cost solvent, dimethyl sulfoxide. Surface transformation on Cu substrate plays a critical role in facilitating the dendrite-free deposition process, which lowers the diffusion energy barrier of the Zn atoms, leading to a uniform and compact thin film for zinc plating. Furthermore, in situ electrochemical atomic force microscopy reveals the plating process via a layer-by-layer growth mechanism and the stripping process through an edge-dissolution mechanism. In addition, Zn||Mo6 S8 full cells exhibit excellent electrochemical performance in terms of cycling stability and rate capability. This work presents a new opportunity to develop nonaqueous rechargeable zinc batteries.