A New Rat Model of Sacral Cord Injury Producing a Neurogenic Bladder and Its Functional and Mechanistic Studies.

Sacral spinal cord injury (SSCI) can disrupt bladder neuromodulation and impair detrusor function. Current studies provide limited information on the histologic and genetic changes associated with SSCI-related neurogenic lower urinary tract dysfunction (NLUTD), resulting in few treatment options. This study aimed to establish a simple animal model of SSCI to better understand the disease progression. Ninety 8-week-old Sprague-Dawley (SD) rats were randomly separated into sham operation and SSCI groups. The SSCI group underwent sacral spinal cord injury, while the sham group did not. Urodynamic and histological assessments were conducted at various intervals (1, 2, 3, 4, and 6 weeks) post-injury to elucidate the disease process. Urodynamic examinations revealed significant bladder dysfunction in the SSCI group compared to the sham group, stabilizing around 3-4 weeks post-injury. Histological examination, including hematoxylin-eosin and Masson's trichrome staining, correlated these functional changes with bladder microstructural alterations. RNA-seq was performed on bladder tissues from the sham group and SSCI group at 6 weeks to identify differentially expressed genes and pathways. Selected genes were further analyzed using polymerase chain reaction (PCR). The findings indicated a pronounced inflammatory response in the first 2 weeks post-SSCI, progressing to bladder fibrosis at 3-4 weeks. In conclusion, this study presents a reliable, reproducible, and straightforward SSCI model, providing insights into bladder functional and morphological alterations post-SSCI and laying the groundwork for future therapeutic research.

Gut microbiota and renal fibrosis.

Renal fibrosis represents a critical pathological condition in the progression of renal dysfunction, characterized by aberrant accumulation of extracellular matrix (ECM) and structural alterations in renal tissue. Recent research has highlighted the potential significance of gut microbiota and demonstrated their influence on host health and disease mechanisms through the production of bioactive metabolites. This review examines the role of alterations in gut microbial composition and their metabolites in the pathophysiological processes underlying renal fibrosis. It delineates current therapeutic interventions aimed at modulating gut microbiota composition, encompassing dietary modifications, pharmacological approaches, and probiotic supplementation, while evaluating their efficacy in mitigating renal fibrosis. Through a comprehensive analysis of current research findings, this review enhances our understanding of the bidirectional interaction between gut microbiota and renal fibrosis, establishing a theoretical foundation for future research directions and potential clinical applications in this domain.

Endoplasmic Reticulum Stress-Mediated Cell Death in Renal Fibrosis.

The endoplasmic reticulum (ER) is indispensable for maintaining normal life activities. Dysregulation of the ER function results in the accumulation of harmful proteins and lipids and the disruption of intracellular signaling pathways, leading to cellular dysfunction and eventual death. Protein misfolding within the ER disrupts its delicate balance, resulting in the accumulation of misfolded or unfolded proteins, a condition known as endoplasmic reticulum stress (ERS). Renal fibrosis, characterized by the aberrant proliferation of fibrotic tissue in the renal interstitium, stands as a grave consequence of numerous kidney disorders, precipitating a gradual decline in renal function. Renal fibrosis is a serious complication of many kidney conditions and is characterized by the overgrowth of fibrotic tissue in the glomerular and tubular interstitium, leading to the progressive failure of renal function. Studies have shown that, during the onset and progression of kidney disease, ERS causes various problems in the kidneys, a process that can lead to kidney fibrosis. This article elucidates the underlying intracellular signaling pathways modulated by ERS, delineating its role in triggering diverse forms of cell death. Additionally, it comprehensively explores a spectrum of potential pharmacological agents and molecular interventions aimed at mitigating ERS, thereby charting novel research avenues and therapeutic advancements in the management of renal fibrosis.

A Novel Microbial Compound Inhibitor and Its Efficacy in Preventing and Controlling Mine Fire Risks: A Case Study on Low-Rank Coal Spontaneous Combustion.

To guarantee the safety and sustainability of coal mining by effectively mitigating the substantial risk associated with coal spontaneous combustion, this study proposes a multifaceted prevention strategy aligned with green environmental principles. A compound flame retardant with a physicochemical control mechanism was prepared using indigenous microorganisms to mineralize residual coal after mining, utilizing Bacillus pasteurelli as a substitute material for inorganic salts. Under laboratory conditions simulating coal self-combustion, biobased flame retardants were employed to investigate the physical and chemical transformations of heat and mass evolution from ambient temperature to combustion in two representative low-rank coals. By quantitatively comparing alterations in microbiome-based groups among raw lignite, bioretarded lignite, and two control samples, the inhibitory mechanism of biobased materials on the oxygen reaction pathway was elucidated. The findings substantiated that biobased modification can consolidate the methyl and methylene groups present in aliphatic hydrocarbon side chains, which are prone to instigating low-temperature oxidation reactions. Additionally, the preventive performance of biobased flame retardants was assessed through temperature-programmed experiments, which involved estimating the critical self-heating temperature, oxygen consumption, and gas production rates of compared coal samples. The results demonstrated significant enhancements in the resistance to spontaneous combustion following bioretarded modification. Notably, the identification grade of long flame coal shifted from easy to moderate susceptibility to spontaneous combustion. Furthermore, biobased flame retardants exhibited remarkable flame retardancy rates of approximately 80% for lignite, thereby validating their efficacy as more environmentally friendly and technologically advanced substitute materials for inhibiting spontaneous combustion in low-rank coals.

Preparation and Application of Co-Doped Zinc Oxide: A Review.

Due to a wide band gap and large exciton binding energy, zinc oxide (ZnO) is currently receiving much attention in various areas, and can be prepared in various forms including nanorods, nanowires, nanoflowers, and so on. The reliability of ZnO produced by a single dopant is unstable, which in turn promotes the development of co-doping techniques. Co-doping is a very promising technique to effectively modulate the optical, electrical, magnetic, and photocatalytic properties of ZnO, as well as the ability to form various structures. In this paper, the important advances in co-doped ZnO nanomaterials are summarized, as well as the preparation of co-doped ZnO nanomaterials by using different methods, including hydrothermal, solvothermal, sol-gel, and acoustic chemistry. In addition, the wide range of applications of co-doped ZnO nanomaterials in photocatalysis, solar cells, gas sensors, and biomedicine are discussed. Finally, the challenges and future prospects in the field of co-doped ZnO nanomaterials are also elucidated.

Targeted Drug Therapy for Senescent Cells Alleviates Unilateral Ureteral Obstruction-Induced Renal Injury in Rats.

Hydronephrosis resulting from unilateral ureteral obstruction (UUO) is a common cause of renal injury, often progressing to late-stage renal fibrosis or even potential renal failure. Renal injury and repair processes are accompanied by changes in cellular senescence phenotypes. However, the mechanism is poorly understood. The purpose of this study is to clarify the changes in senescence phenotype at different time points in renal disease caused by UUO and to further investigate whether eliminating senescent cells using the anti-senescence drug ABT263 could attenuate UUO-induced renal disease. Specifically, renal tissues were collected from established UUO rat models on days 1, 2, 7, and 14. The extent of renal tissue injury and fibrosis in rats was assessed using histological examination, serum creatinine, and blood urea nitrogen levels. The apoptotic and proliferative capacities of renal tissues and phenotypic changes in cellular senescence were evaluated. After the intervention of the anti-senescence drug ABT263, the cellular senescence as well as tissue damage changes were re-assessed. We found that before the drug intervention, the UUO rats showed significantly declined renal function, accompanied by renal tubular injury, increased inflammatory response, and oxidative stress, alongside aggravated cellular senescence. Meanwhile, after the treatment with ABT263, the rats had a significantly lower number of senescent cells, attenuated renal tubular injury and apoptosis, enhanced proliferation, reduced oxidative stress and inflammation, improved renal function, and markedly inhibited fibrosis. This suggests that the use of the anti-senescence drug ABT263 to eliminate senescent cells can effectively attenuate UUO-induced renal injury. This highlights the critical role of cellular senescence in the transformation of acute injury into chronic fibrosis.

The role of mitophagy in the development of chronic kidney disease.

Chronic kidney disease (CKD) represents a significant global health concern, with renal fibrosis emerging as a prevalent and ultimate manifestation of this condition. The absence of targeted therapies presents an ongoing and substantial challenge. Accumulating evidence suggests that the integrity and functionality of mitochondria within renal tubular epithelial cells (RTECs) often become compromised during CKD development, playing a pivotal role in the progression of renal fibrosis. Mitophagy, a specific form of autophagy, assumes responsibility for eliminating damaged mitochondria to uphold mitochondrial equilibrium. Dysregulated mitophagy not only correlates with disrupted mitochondrial dynamics but also contributes to the advancement of renal fibrosis in CKD. While numerous studies have examined mitochondrial metabolism, ROS (reactive oxygen species) production, inflammation, and apoptosis in kidney diseases, the precise pathogenic mechanisms underlying mitophagy in CKD remain elusive. The exact mechanisms through which modulating mitophagy mitigates renal fibrosis, as well as its influence on CKD progression and prognosis, have not undergone systematic investigation. The role of mitophagy in AKI has been relatively clear, but the role of mitophagy in CKD is still rare. This article presents a comprehensive review of the current state of research on regulating mitophagy as a potential treatment for CKD. The objective is to provide fresh perspectives, viable strategies, and practical insights into CKD therapy, thereby contributing to the enhancement of human living conditions and patient well-being.

Cellular senescence in acute kidney injury: Target and opportunity.

Acute kidney injury (AKI) is a common clinical disease with a high incidence and mortality rate. It typically arises from hemodynamic alterations, sepsis, contrast agents, and toxic drugs, instigating a series of events that culminate in tissue and renal damage. This sequence of processes often leads to acute renal impairment, prompting the initiation of a repair response. Cellular senescence is an irreversible arrest of the cell cycle. Studies have shown that renal cellular senescence is closely associated with AKI through several mechanisms, including the promotion of oxidative stress and inflammatory response, telomere shortening, and the down-regulation of klotho expression. Exploring the role of cellular senescence in AKI provides innovative therapeutic ideas for both the prevention and treatment of AKI. Furthermore, it has been observed that targeted removal of senescent cells in vivo can efficiently postpone senescence, resulting in an enhanced prognosis for diseases associated with senescence. This article explores the effects of common anti-senescence drugs senolytics and senostatic and lifestyle interventions on renal diseases, and mentions the rapid development of mesenchymal stem cells (MSCs). These studies have taken senescence-related research to a new level. Overall, this article comprehensively summarizes the studies on cellular senescence in AKI, aiming is to elucidate the relationship between cellular senescence and AKI, and explore treatment strategies to improve the prognosis of AKI.

Cisplatin induces acute kidney injury by downregulating miR-30e-5p that targets Galnt3 to activate the AMPK signaling pathway.

Cisplatin nephrotoxicity is an etiological factor for acute kidney injury (AKI). MicroRNA (miRNA) expression is dysregulated in cisplatin-induced AKI (cAKI) although the underlying mechanisms are unclear. A cAKI model was established by intraperitoneally injecting cisplatin, and key miRNAs were screened using high-throughput miRNA sequencing. The functions of key miRNAs were determined using the cell viability, live/dead, reactive oxygen species (ROS), and 5-ethynyl-2'-deoxyuridine (EdU) proliferation assays. Additionally, the macrophage membrane was wrapped around a metal-organic framework (MOF) loaded with miRNA agomir to develop a novel composite material, macrophage/MOF/miRNA agomir nanoparticles (MMA NPs). High-throughput miRNA sequencing revealed that miR-30e-5p is a key miRNA that is downregulated in cAKI. The results of in vitro experiments demonstrated that miR-30e-5p overexpression partially suppressed the cisplatin-induced or lipopolysaccharide (LPS)-induced downregulation of cell viability, proliferation, upregulation of ROS production, and cell death. Meanwhile, the results of in vivo and in vitro experiments demonstrated that MMA NPs alleviated cAKI by exerting anti-inflammatory effects. Mechanistically, cisplatin downregulates the expression of miR-30e-5p, and the downregulated miR-30e-5p can target Galnt3 to activate the adenosine 5'-monophosphate activated protein kinase (AMPK) signaling pathway, which promotes the progression of AKI. Our study found that miR-30e-5p is a key downregulated miRNA in cAKI. The downregulated miR-30e-5p promotes AKI progression by targeting Galnt3 to activate the AMPK signaling pathway. The newly developed MMA NPs were found to have protective effects on cAKI, suggesting a potential novel strategy for preventing cAKI.

Association between grip strength and stress urinary incontinence of NHANES 2011-2014.

OBJECTIVES: To investigate the association between grip strength (GS) and relative grip strength (rGS) with the prevalence and severity risk of SUI. METHODS: Female patients were retrieved from the NHANES 2011-2014. GS was measured using a digital hand dynamometer, rGS was defined as grip strength divided by BMI. Samples were classified into four groups based on quartiles of GS and rGS distribution (Q1-Q4)。Logistic regression models were established to detect the relationship between GS or rGS and SUI. The potential bias of baseline variables between SUI and non-SUI groups was controlled by performing the propensity score matching (PSM). RESULTS: A total of 4263 samples were included, with 3085 (85%) people in non-SUI group and 1178 (27.6%) people in SUI group. GS and rGS levels of people without SUI were higher than that of SUI patients. Monthly SUI patients' GS and rGS levels were higher than weekly SUI patients' level. Logistic regression analysis showed that risks of prevalence and severity of SUI decreased with increasing levels of GS and rGS. rGS was found to have a stronger association with SUI than GS [prevalence: GS: Q4 vs. Q1: aOR = 0.633, 95%CI = 0.508-0.789, p < 0.001; rGS: Q4 vs. Q1: aOR = 0.365, 95%CI = 0.290-0.459, p < 0.001; severity: GS: Q4 vs. Q1: aOR = 0.727, 95%CI = 0.600-0.881, p = 0.001; rGS: Q4 vs. Q1: aOR = 0.371, 95%CI = 0.282-0.488, p < 0.001]. The results of PSM confirmed that GS and rGS were correlated with SUI. CONCLUSIONS: Lower levels of GS and rGS are associated with an increased prevalence and severity risk of SUI.

Small Molecule Cocktails Promote Fibroblast-to-Leydig-like Cell Conversion for Hypogonadism Therapy.

Male hypogonadism arises from the inadequate production of testosterone (T) by the testes, primarily due to Leydig cell (LC) dysfunction. Small molecules possess several advantages, including high cell permeability, ease of synthesis, standardization, and low effective concentration. Recent investigations have illuminated the potential of small molecule combinations to facilitate direct lineage reprogramming, removing the need for transgenes by modulating cellular signaling pathways and epigenetic modifications. In this study, we have identified a specific cocktail of small molecules, comprising forskolin, DAPT, purmorphamine, 8-Br-cAMP, 20α-hydroxycholesterol, and SAG, capable of promoting the conversion of fibroblasts into Leydig-like cells (LLCs). These LLCs expressed key genes involved in testosterone synthesis, such as Star, Cyp11a1, and Hsd3b1, and exhibited the ability to secrete testosterone in vitro. Furthermore, they successfully restored serum testosterone levels in testosterone-castrated mice in vivo. The small molecule cocktails also induced alterations in the epigenetic marks, specifically H3K4me3, and enhanced chromosomal accessibility on core steroidogenesis genes. This study presents a reliable methodology for generating Leydig-like seed cells that holds promise as a novel therapeutic approach for hypogonadism.

A dual drug-loaded peptide system with morphological transformation prolongs drug retention and inhibits breast cancer growth.

The treatment of breast cancer relies heavily on chemotherapy, but chemotherapy is limited by the disadvantages of poor targeting, susceptibility to extracellular matrix (ECM) interference and a short duration of action in tumor cells. To address these limitations, we developed an amphipathic peptide containing an RGD motif, Pep1, that encapsulated paclitaxel (PTX) and losartan potassium (LP) to form the drug-loaded peptide PL/Pep1. PL/Pep1 self-assembled into spherical nanoparticles (NPs) under normal physiological conditions and transformed into aggregates containing short nanofibers at acidic pH. The RGD peptide facilitated tumor targeting and the aggregates prolonged drug retention in the tumor, which allowed more drug to reach and accumulate in the tumor tissue to promote apoptosis and remodel the tumor microenvironment. The results of in vitro and in vivo experiments confirmed the superiority of PL/Pep1 in terms of targeting, prolonged retention and facilitated penetration for antitumor therapy. In conclusion, amphipathic peptides as coloaded drug carriers are a new platform and strategy for breast cancer chemotherapy.

Machine learning assisted interpretation of 2D solid-state nuclear magnetic resonance spectra.

A machine learning methodology using deep neural network (DNN) for interpreting multidimensional solid-state nuclear magnetic resonance (SSNMR) of various synthetic and natural polymers is presented. The separated local field (SLF) SSNMR which correlates local well-defined heteronuclear dipolar with the tensor orientation of the chemical shift anisotropy (CSA) of spin in the solid state can provide valuable structure and molecular dynamics information of synthetic and biopolymers. Compared with the traditional linear least-square fitting, the proposed DNN-based methodology can efficiently and accurately determine the tensor orientation of CSA of both 13C and 15N in all four samples. The method achieves prediction precisions of the Euler angles with < ±5° and is characterized by low training costs and high efficiency (<1 s). The feasibility and robustness of the DNN-based analysis methodology are confirmed by comparison to reported-literature values. This strategy is expected to aid in the interpretation of complex multidimensional NMR spectra of complicated polymer system.

Synergistic Effect of P Doping and Mo-Ni-Based Heterostructure Electrocatalyst for Overall Water Splitting.

Heterostructure construction and heteroatom doping are powerful strategies for enhancing the electrolytic efficiency of electrocatalysts for overall water splitting. Herein, we present a P-doped MoS2/Ni3S2 electrocatalyst on nickel foam (NF) prepared using a one-step hydrothermal method. The optimized P[0.9mM]-MoS2/Ni3S2@NF exhibits a cluster nanoflower-like morphology, which promotes the synergistic electrocatalytic effect of the heterostructures with abundant active centers, resulting in high catalytic activity for the hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) in alkaline electrolyte. The electrode exhibits low overpotentials and Tafel slopes for the HER and OER. In addition, the catalyst electrode used in a two-electrode system for overall water splitting requires an ultralow voltage of 1.42 V at 10 mA·cm-2 and shows no obvious increase in current within 35 h, indicating excellent stability. Therefore, the combination of P doping and the heterostructure suggests a novel path to formulate high-performance electrocatalysts for overall water splitting.

A new application of multiplex PCR combined with membrane biochip assay for rapid detection of 9 common pathogens in sepsis.

Rapid and accurate identification of specific sepsis pathogens is critical for patient treatment and disease control. This study aimed to establish a new application for the rapid identification of common pathogens in patients with suspected sepsis and evaluate its role in clinical application. A multiplex PCR assay was designed to simultaneously amplify specific conserved regions of nine common pathogenic microorganisms in sepsis, including Acinetobacter baumannii, Escherichia coli, Klebsiella pneumonia, Pseudomonas aeruginosa, Enterococcus faecalis, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumonia, and Candida albicans. The PCR products were analyzed by a membrane biochip. The analytical sensitivity of the assay was determined at a range of 5-100 copies/reaction for each standard strain, and the detection range was 20-200 cfu/reaction in a series dilution of simulated clinical samples at different concentrations. Out of the 179 clinical samples, the positive rate for pathogens detected by the membrane biochip assay and blood culture method was 20.11% (36/179) and 18.44% (33/179), respectively. However, by comparing the positive rate of the nine common pathogens we detected, the membrane biochip assay tended to be more sensitive than the blood culture method (20.11% vs 15.64%). The clinical sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the membrane biochip assay were 92.9%, 93.2%, 72.2% and 98.6%, respectively. Generally, this multiplex PCR combined membrane biochip assay can be used to detect major sepsis pathogens, and is useful for early initiation of effective antimicrobial treatment, and is feasible for sepsis pathogens identification in routine clinical practice.

Heterocyclic Aromatic Amines and Risk of Kidney Stones: A Cross-Sectional Study in US Adults.

Background: Heterocyclic aromatic amines (HAAs) are a group of harmful substances produced while cooking meat at high temperatures. This study aimed to investigate the relationship between HAAs and the occurrence of kidney stones. Methods: Data on the level of four HAAs, including 2-Amino-9H-pyrido [2, 3-b] indole (A-α-C), 1-Methyl-9H-pyrido [3, 4-b] indole (Harman), 9H-Pyrido [3, 4-b] indole (Norharman), and 2-Amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine (PhIP), in the urine from adult participants were extracted from the 2013-2014 NHANES database. Propensity score matching (PSM) was used to balance confounding variables between the stone former and non-stone former groups, and logistic regression analysis was performed to analyze the relationship between HAAs and the occurrence of kidney stones. Results: Of the 1,558 eligible participants, a history of kidney stones was self-reported by 140 (9.0%). Compared to non-stone formers, stone formers had higher concentrations of A-α-C, Harman, and Norharman and lower concentrations of PhlP in urine. After adjusting for all other confounding variables, multivariate logistic regression analysis showed that the high-Harman group had a higher risk of kidney stones than the low-Harman group [adjusted odds ratios (aOR) = 1.618, 95% CI: 1.076-2.433, p = 0.021]. After PSM analysis, Harman concentration remained a risk factor for kidney stones (high-Harman group vs. low-Harman group: aOR = 1.951, 95% CI: 1.059-3.596, p = 0.032). Conclusion: Increased urinary Harman concentrations are associated with an increased risk of kidney stones in the general US population.

Physical Activity Reduces the Effect of High Body Mass Index on Kidney Stones in Diabetes Participants From the 2007-2018 NHANES Cycles: A Cross-Sectional Study.

Background: Body mass index (BMI) is a vital risk factor for kidney stones, but physical activity may reduce the incidence of kidney stones. However, it remains unknown whether physical activity reduces the effect of high BMI on kidney stones in diabetes participants. Methods: We included clinical information from 4,008 adult participants with diabetes from the National Health and Nutrition Examination Survey (NHANES) database from 2007 to 2018. Univariate and multivariate logistic regression analyses were used to analyze the relationship between BMI and kidney stones, as well as the risk of BMI and kidney stones in different physical activity subgroups. Results: A total of 4,008 diabetic participants were included in this study, of whom 652 (16.3%) self-reported a history of kidney stones. Logistic regression analysis showed a positive association between BMI and kidney stones. After adjusting for other confounders, the adjusted ORs for the risk of kidney stones was 1.514 (95% CI, 1.134-2.022, p = 0.005) for participants with BMI ≥30 kg/m2 among all participants; the risk of kidney stones was elevated (OR = 1.572, 95% CI, 1.134-2.022, p = 0.005) in group without physical activity, and a reduced risk (OR = 1.421, 95% CI, 0.847-2.382, p = 0.183) in the group with physical activity. Furthermore, similar results were found in most subgroups. Conclusion: Our study suggests that high BMI is a risk factor for diabetes kidney stone participants and that physical activity may moderate this relationship to some extent.

Renal denervation alleviates renal ischemic reperfusion injury-induced acute and chronic kidney injury in rats partly by modulating miRNAs.

BACKGROUND: Renal denervation (RDN) has been used to promote kidney injury repair, whereas miRNAs have been found to be involved in the pathophysiology of renal injury. However, the miRNA alterations that occur after RDN and the related protective mechanisms remain to be determined. METHODS: Renal ischemic reperfusion injury (IRI) rat model was established and RDN was performed. Animals were killed at 24 h and 2 weeks following the operation. Tyrosine hydroxylase (TH) levels, renal function, tubular cell apoptosis and histological sections were examined at 24 h, whereas renal fibrosis and capillary vessels were assessed at 2 weeks. Furthermore, the expression of miRNAs in the injured kidney was determined using micro-array and the target genes were analyzed. RESULTS: We found that TH was eliminated and that renal function was improved in the denervation group at 24 h. RDN reduced tubular cell apoptosis and mitigated the histological lesion. Furthermore, an increase of capillary vessel density and reduction of renal fibrosis were observed after 2 weeks. Moreover, the numbers of miRNAs were up-regulated after RDN treatment, and the miRNAs targeted pro-angiogenic, anti-fibrotic and inflammatory pathways. CONCLUSIONS: RDN is a reliable method for alleviating IRI-induced acute and chronic kidney injury, and modulating the miRNA-related pro-angiogenic, anti-fibrotic or inflammatory pathways involved in this process.

Multi-Risk Assessment of Mine Lithium Battery Fire Based on Quantitative Factor Characterization.

As a large number of new energy is employed as the driving force for the operation and transportation machinery of underground space projects, the lithium battery load in confined spaces, such as working faces, roadways and tunnels increases in geometric progression, and the coupled risks of heat damage and smoke poisoning caused by possible fires become more serious. In this paper, experimental and numerical methods were implemented to study the propagation mechanism of heat- and mass-induced disasters under catastrophic conditions, and a quantitative characterization model of multiple risk factors of thermal runaway and toxic gas diffusion of battery fire was proposed. The fuzzy analytical hierarchy process (FAHP) was conducted to calculate and grade the risk of lithium battery fire in a typical mine working face under multiple factors, including hazard source, personnel, working environment and emergency response. In addition, a quantitative early warning and control model was established for identified high-risk probability events. The results promote the quantitative and scientific development of multiple risk assessment and decision-making of confined space fire.

Ability of volume measures of hydronephrosis to predict need for surgery and evaluate renal function in children with ureteropelvic junction obstruction.

OBJECTIVE: To explore the efficacy of quantitative renal volume measures on magnetic resonance urography images in predicting need for surgery among children with ureteropelvic junction obstruction and their ability to evaluate renal function. METHODS: A total of 88 cases of hydronephrosis in 50 patients were collected between 1 April 2018 and 31 March 2020, including 30 operated kidney and 58 unoperated kidney cases. Clinical data were collected, and quantitative analysis of magnetic resonance urography was performed. Renal volume, hydronephrosis volume and the volume ratio of hydronephrosis (hydronephrosis volume/renal volume) were measured and calculated. We analyzed the relationships between the above indices in the two groups and compared these with renal function. RESULTS: Compared with the unoperated kidney group, hydronephrosis volume, renal volume and hydronephrosis volume/renal volume of the operated kidney group increased significantly. Hydronephrosis volume (area under the curve 0.972, 95% confidence interval 0.943-1.000; P < 0.001) and hydronephrosis volume/renal volume (area under the curve 0.968, 95% confidence interval 0.939-0.998; P < 0.001) were superior to ultrasonography and renal function examination in predicting the probability of surgery, and their sensitivity values (hydronephrosis volume/renal volume: 96.67%; hydronephrosis volume: 93.33%) were higher than those of the renal function test (50%). There was a significant difference among different renal function groups in the pairwise comparison of hydronephrosis volume and hydronephrosis volume/renal volume (P < 0.05). CONCLUSION: Quantitative volume measures of hydronephrosis by magnetic resonance urography had a greater ability to predict need for surgery than ultrasonography and dynamic renal imaging, and it can be used as method by which to evaluate surgery. Hydronephrosis volume and hydronephrosis volume/renal volume have greater predictive ability, and play an important role in the deterioration of renal function.