Risk Factors, Incidence, and Outcomes Associated With Clinically Significant Airway Ischemia.

Airway complications following lung transplantation remain an important cause of morbidity and mortality. We aimed to identify the incidence, risk factors and outcomes associated with clinically significant airway ischemia (CSAI) in our center. We reviewed 217 lung transplants (386 airway anastomoses) performed at our institution between February 2016 and December 2020. Airway images were graded using the 2018 ISHLT grading guidelines modified slightly for retrospective analysis. Airways were considered to have CSAI if they developed ischemia severity >B2, stenosis >50%, and/or any degree of dehiscence within 6-months of transplant. Regression analyses were used to evaluate outcomes and risk factors for CSAI. Eighty-two patients (37.8%) met criteria for CSAI. Of these, twenty-six (32%) developed stenosis and/or dehiscence, and 17 (21%) required interventions. Patients with CSAI had lower one-year (80.5% vs. 91.9%, p = 0.05) and three-year (67.1% vs. 77.8%, p = 0.08) survival than patients without CSAI. Factors associated with CSAI included younger recipient age, recipient diabetes, single running suture technique, performance of the left anastomosis first, lower venous oxygen saturation within 48-h, and takeback for major bleeding. Our single-center analysis suggests that airway ischemia remains a major obstacle in contemporary lung transplantation. Improving the local healing milieu of the airway anastomosis could potentially mitigate this risk.

Optimization of Fuzzy Control Parameters for Wind Farms and Battery Energy Storage Systems Based on an Enhanced Artificial Bee Colony Algorithm under Multi-Source Sensor Data.

With the rapid development of sensors and other devices, precise control for the generation of new energy, especially in the context of highly stochastic wind power generation, has been strongly supported. However, large-scale wind farm grid connection can cause the power system to enter a low inertia state, leading to frequency instability. Battery energy storage systems (BESSs) have the advantages of a fast response speed and high flexibility, and can be applied to wind farm systems to improve the frequency fluctuation problem in the process of grid connection. To address the frequency fluctuation problem caused by the parameter error of the fuzzy membership function in the fuzzy control of a doubly fed induction generator (DFIG) and a BESS, this paper proposes an improved Artificial Bee Colony (ABC) algorithm based on multi-source sensor data for optimizing the fuzzy controller to improve the frequency control ability of BESSs and DFIGs. A Gaussian wandering mechanism was introduced to improve the ABC algorithm and enhance the convergence speed of the algorithm, and the improved ABC algorithm was optimized for the selection of fuzzy control affiliation function parameters to improve the frequency response performance. The effectiveness of the proposed control strategy was verified on the MATLAB/Simulink simulation platform. After optimization using the proposed control strategy, the oscillation amplitude was reduced by 0.15 Hz, the precision was increased by 40%, and the steady-state frequency deviation was reduced by 26%. The results show that the method proposed in this paper provides a great improvement in the frequency stability of coordinated systems of wind farms and BESSs.

Novel recombinant R-spondin1 promotes hair regeneration by targeting the Wnt/ß-catenin signaling pathway.

Roof plate-specific spondin 1 (R-spondin1, RSPO1) is a Wnt/ß-catenin signaling pathway activator that binds with Wnt ligands to stimulate the Wnt/ß-catenin signaling pathway, which is key to hair regeneration. However, it is not clear whether recombinant RSPO1 (rRSPO1) affects hair regeneration. Here, we treat C57BL/6 male mice with rRSPO1 and investigate the expression of the Wnt/ß-catenin signaling pathway and the activation of hair follicle stem cells in the dorsal skin. The mouse skin color score and hair-covered area are determined to describe hair growth, and the skin samples are subjected to H&E staining, western blot analysis and immunofluorescence staining to evaluate hair follicle development and the expressions of Wnt/ß-catenin signaling pathway-related proteins. We find that rRSPO1 activates mouse hair follicle stem cells (mHFSCs) and accelerates hair regeneration. rRSPO1 increases the hair-covered area, the number of hair follicles, and the hair follicle diameter and length. Moreover, rRSPO1 enhances the activity of Wnt/ß-catenin signaling pathway-related proteins and the expressions of HFSC markers, as well as mHFSC viability. These results indicate that subcutaneous injection of rRSPO1 can improve hair follicle development by activating the Wnt/ß-catenin signaling pathway, thereby promoting hair regeneration. This study demonstrates that rRSPO1 has the potential to treat hair loss by activating the Wnt/ß-catenin signaling pathway.

Mechanism and restoration strategy of lysosomal abnormalities induced by urinary protein overload in proximal tubule epithelial cells.

BACKGROUND: Persistent elevated concentrations of urinary protein can destroy proximal tubule epithelial cells (PTECs) by inducing lysosomal abnormalities, thereby aggravating PTEC damage and renal fibrosis. However, the specific mechanisms of these serial biochemical events and methods for treating or preventing PTEC damage upon proteinuria need further investigation. RESULTS: In this study, electron microscopy and dual-labeled immunofluorescence analysis for identifying lysosome type revealed inadequate primary lysosome biogenesis and secondary lysosome accumulation in the PTECs of patients with minimal change nephrotic syndrome or membranous nephropathy who suffered from proteinuria. In vitro studies on HK-2 cells indicated that this abnormality was associated with decreased expression of transcription factor EB (TFEB). In contrast, TFEB overexpressing HK-2 cells under urinary protein overload exhibited significantly reduced accumulation of secondary lysosomes and increased proportion and quantity of primary lysosomes as indicated by dual-labeled immunofluorescence. Further, these cells could upregulate lysosomal degradation functions, as determined using Cathepsin L activity assays and flow cytometry for dye quenched-albumin. CONCLUSIONS: These results indicate that abnormal TFEB expression is a key mechanism of lysosomal dyshomeostasis caused by protein overload in PTECs. TFEB is thus a potential therapeutic target for the treatment of urinary protein-related kidney disease.

Tactile priming accelerates conscious access to continuous flash-suppressed characters.

NEW FINDINGS: What is the central question of this study? Research has reported that some sensory input, such as auditory and olfactory input, can affect subliminal visual processing. However, it is important to address whether tactile input, another form of elementary sensory input, could influence the interocular rivalry process. What is the main finding and its importance? We present several pieces of evidence regarding the influences of familiar tactile shapes and temperature on continuous flash suppression. Our findings provide support for the hypothesis that there is a cross-modal effect on subconscious visual semantic processing of Chinese characters. More specifically, tactile sensations affect subliminal processing of visual information. ABSTRACT: Tactile and visual sensations are the most vital human functions for obtaining environmental information. However, whether tactile information influences visual processing remains unclear. In this study, a breaking continuous flash suppression (b-CFS) protocol was used to measure the extent to which tactile sensations facilitate visual processing subconsciously. In experiment 1, finger stimulation with cold and hot temperatures served as primers for the words 'cold' and 'hot', which were in turn suppressed by CFS. In experiment 2, subjects viewed the upright or inverted word 'cell phone', with or without tactile priming of holding a cell phone in their hand. Results demonstrated that the tactile primer significantly shortened the reaction time in the touch group compared with the control group in both experiments. Thus, the tactile sensation of a familiar article and/or temperature appears to facilitate corresponding visual semantic recognition to break CFS earlier.

Regulation of Monocarboxylic Acid Transporter 1 Trafficking by the Canonical Wnt/ß-Catenin Pathway in Rat Brain Endothelial Cells Requires Cross-talk with Notch Signaling.

The transport of monocarboxylate fuels such as lactate, pyruvate, and ketone bodies across brain endothelial cells is mediated by monocarboxylic acid transporter 1 (MCT1). Although the canonical Wnt/ß-catenin pathway is required for rodent blood-brain barrier development and for the expression of associated nutrient transporters, the role of this pathway in the regulation of brain endothelial MCT1 is unknown. Here we report expression of nine members of the frizzled receptor family by the RBE4 rat brain endothelial cell line. Furthermore, activation of the canonical Wnt/ß-catenin pathway in RBE4 cells via nuclear ß-catenin signaling with LiCl does not alter brain endothelialMct1mRNA but increases the amount of MCT1 transporter protein. Plasma membrane biotinylation studies and confocal microscopic examination of mCherry-tagged MCT1 indicate that increased transporter results from reduced MCT1 trafficking from the plasma membrane via the endosomal/lysosomal pathway and is facilitated by decreased MCT1 ubiquitination following LiCl treatment. Inhibition of the Notch pathway by the γ-secretase inhibitorN-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycinet-butyl ester negated the up-regulation of MCT1 by LiCl, demonstrating a cross-talk between the canonical Wnt/ß-catenin and Notch pathways. Our results are important because they show, for the first time, the regulation of MCT1 in cerebrovascular endothelial cells by the multifunctional canonical Wnt/ß-catenin and Notch signaling pathways.

Hyperglycemia repression of miR-24 coordinately upregulates endothelial cell expression and secretion of von Willebrand factor.

An elevated level of von Willebrand factor (VWF) in diabetic patients is associated with increased risk of thrombotic cardiovascular events. The underlying mechanism of how VWF expression is upregulated in diabetes mellitus is poorly understood. We now report that hyperglycemia-induced repression of microRNA-24 (miR-24) increases VWF expression and secretion in diabetes mellitus. In diabetic patients and diabetic mouse models (streptozotocin/high-fat diet-induced and db/db mice), miR-24 is reduced in both tissues and plasma. Knockdown of miR-24 in mice leads to increased VWF mRNA and protein levels and enhanced platelet tethering (spontaneous thrombosis). miR-24 tightly controls VWF levels through pleiotropic effects, including direct binding to the 3' untranslated region of VWF and targeting FURIN and the histamine H1 receptor, known regulators of VWF processing and secretion in endothelial cells. We present a novel mechanism for miR-24 downregulation through hyperglycemia-induced activation of aldose reductase, reactive oxygen species, and c-Myc. These findings support a critical role for hyperglycemic repression of miR-24 in VWF-induced pathology. miR-24 represents a novel therapeutic target to prevent adverse thrombotic events in patients with diabetes mellitus.

Comparative efficacy of different exercise methods to improve cardiopulmonary function in stroke patients: a network meta-analysis of randomized controlled trials.

Background: Although some studies have shown that exercise has a good effect on improving the cardiopulmonary function of stroke patients, it still needs to be determined which exercise method does this more effectively. We, therefore, aimed to evaluate the effectiveness of different exercise methods in improving cardiovascular function in stroke patients through a network meta-analysis (NMA), providing a basis to select the best treatment plan for stroke patients. Methods: We systematically searched CNKI, WanFang, VIP, CBM, PubMed, Embase, Web of Science, and The Cochrane Library databases from establishment to 30 April 2023. Randomized controlled trials (RCTS) on exercise improving cardiopulmonary function in stroke patients were included, and we screened the included articles and extracted the relevant data. RevMan (version 5.4) and Stata (version 17.0) were used for data analysis. Results: We included 35 RCTs and a total of 2,008 subjects. Intervention measures included high-intensity interval training (HIIT), aerobic training (AT), resistance training (RT), combined aerobic and resistance exercise (CE), and conventional therapy (CT). In the network meta-analysis, the surface under the cumulative ranking area (SUCRA) ranking result indicated that HIIT improved peak oxygen uptake (VO2peak) and 6 mins walking distance (6MWD) optimally, with rankings of HIIT (100.0%) > CE (70.5%) > AT (50.2%) > RT (27.7%) > CT (1.6%), and HIIT (90.9%) > RT (60.6%) > AT (48.9%) > RT (48.1%) > CT (1.5%), respectively. The SUCRA ranking result showed that CE improved systolic blood pressure (SBP) and diastolic blood pressure (DBP) optimally, with rankings of CE (82.1%) > HIIT (49.8%) > AT (35.3%) > CT (32.8%), and CE (86.7%) > AT (45.0%) > HIIT (39.5%) > CT (28.8%), respectively. Conclusion: We showed that exercise can effectively improve the cardiopulmonary function of stroke patients. HIIT was the most effective in improving VO2peak and 6MWD in stroke patients. CE was the most effective in improving SBP and DBP in stroke patients. However, due to the limitations of existing clinical studies and evidence, larger sample size, multi-center, and high-quality RCTs are needed to verify the above conclusions in the future. Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier [CRD42023436773].

Comparative efficacy of different repetitive transcranial magnetic stimulation protocols for lower extremity motor function in stroke patients: a network meta-analysis.

Background: Lower extremity motor dysfunction is one of the most severe consequences after stroke, restricting functional mobility and impairing daily activities. Growing evidence suggests that repetitive transcranial magnetic stimulation (rTMS) can improve stroke patients' lower extremity motor function. However, there is still controversy about the optimal rTMS protocol. Therefore, we compared and analyzed the effects of different rTMS protocols on lower extremity motor function in stroke patients using network meta-analysis (NMA). Methods: We systematically searched CNKI, WanFang, VIP, CBM, PubMed, Embase, Web of Science, and Cochrane Library databases (from origin to 31 December 2023). Randomized controlled trials (RCTs) or crossover RCTs on rTMS improving lower extremity motor function in stroke patients were included. Two authors independently completed article screening, data extraction, and quality assessment. RevMan (version 5.4) and Stata (version 17.0) were used to analyze the data. Results: A total of 38 studies with 2,022 patients were eligible for the NMA. The interventions included HFrTMS-M1, LFrTMS-M1, iTBS-Cerebellum, iTBS-M1, dTMS-M1, and Placebo. The results of NMA showed that LFrTMS-M1 ranked first in FMA-LE and speed, and HFrTMS-M1 ranked first in BBS, TUGT, and MEP amplitude. The subgroup analysis of FMA-LE showed that HFrTMS-M1 was the best stimulation protocol for post-stroke time > 1 month, and LFrTMS-M1 was the best stimulation protocol for post-stroke time ≤ 1 month. Conclusion: Considering the impact of the stroke phase on the lower extremity motor function, the current research evidence shows that HFrTMS-M1 may be the preferred stimulation protocol to improve the lower extremity motor function of patients for post-stroke time > 1 month, and LFrTMS-M1 for post-stroke time ≤ 1 month. However, the above conclusion needs further analysis and validation by more high-quality RCTs.Systematic Review Registration:www.crd.york.ac.uk/prospero/, identifier (CRD42023474215).

Washed microbiota transplantation reduces glycemic variability in unstable diabetes.

BACKGROUND: Dysbiosis of gut microbiota is causally linked to impaired host glucose metabolism. We aimed to study effects of the new method of fecal microbiota transplantation, washed microbiota transplantation (WMT), on reducing glycemic variability (GV) in unstable diabetes. METHODS: Fourteen eligible patients received three allogenic WMTs and were followed up at 1 week, 1 month, and 3 months. Primary outcomes were daily insulin dose, glucose excursions during meal tests, and GV indices calculated from continuous monitoring or self-monitoring glucose values. Secondary outcomes were multiomics data, including 16S rRNA gene sequencing, metagenomics, and metabolomics to explore underlying mechanisms. RESULTS: Daily insulin dose and glucose excursions markedly dropped, whereas GV indices significantly improved up to 1 month. WMT increased gut microbial alpha diversity, beta diversity, and network complexity. Taxonomic changes featured lower abundance of genera Bacteroides and Escherichia-Shigella, and higher abundance of genus Prevotella. Metagenomics functional annotations revealed enrichment of distinct microbial metabolic pathways, including methane biosynthesis, citrate cycle, amino acid degradation, and butyrate production. Derived metabolites correlated significantly with improved GV indices. WMT did not change circulating inflammatory cytokines, enteroendocrine hormones, or C-peptide. CONCLUSIONS: WMT showed strong ameliorating effect on GV, raising the possibility of targeting gut microbiota as an effective regimen to reduce GV in diabetes.

The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury.

Acute kidney injury (AKI) is a common clinical condition associated with high morbidity and mortality. The pathogenesis of AKI has not been fully elucidated, with a lack of effective treatment. Renal tubular epithelial cells (TECs) play an important role in AKI, and their damage and repair largely determine the progression and prognosis of AKI. In recent decades, it has been found that the mitochondria, endoplasmic reticulum (ER), lysosomes, and other organelles in TECs are damaged to varying degrees in AKI, and that they can influence each other through various signaling mechanisms that affect the recovery of TECs. However, the association between these multifaceted signaling platforms, particularly between mitochondria and lysosomes during AKI remains unclear. This review summarizes the specific pathophysiological mechanisms of the main TECs organelles in the context of AKI, particularly the potential interactions among them, in order to provide insights into possible novel treatment strategies.

The kidney-expressed transcription factor ZKSCAN3 is dispensable for autophagy transcriptional regulation and AKI progression in mouse.

Acute kidney injury (AKI) is a common clinical disease that can cause serious harm to the kidneys, but it has no effective treatment till now. The modulation of autophagy pathway regulation is considered a potentially effective therapeutic approach in AKI prevention and treatment. ZKSCAN3 has been shown to be an important transcription factor that negatively regulates autophagy activity in cancer tissues. In order to determine whether autophagy could be activated by knocking out ZKSCAN3 to exert the renal protective effect of autophagy, we constructed AKI models with Zkscan3 knockout (KO) mice and detected renal pathological changes and renal function changes as well as autophagy-related indicators. We found that Zkscan3 KO had no significant effect on kidney development. Besides, no significant changes in autophagy activity were observed under normal physiological or AKI conditions. In non-tumor tissues, ZKSCAN3 did not mediate transcriptional regulation of autophagy-related genes. These findings suggest that because ZKSCAN3 may not function in the transcriptional regulation of autophagy-related genes in non-tumor tissues, it may not be used as a therapeutic target for AKI.

The Role of Parietal Epithelial Cells in the Pathogenesis of Podocytopathy.

Podocytopathy is the most common feature of glomerular disorder characterized by podocyte injury- or dysfunction-induced excessive proteinuria, which ultimately develops into glomerulosclerosis and results in persistent loss of renal function. Due to the lack of self-renewal ability of podocytes, mild podocyte depletion triggers replacement and repair processes mostly driven by stem cells or resident parietal epithelial cells (PECs). In contrast, when podocyte recovery fails, activated PECs contribute to the establishment of glomerular lesions. Increasing evidence suggests that PECs, more than just bystanders, have a crucial role in various podocytopathies, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy, IgA nephropathy, and lupus podocytopathy. In this review, we attempt to dissect the diverse role of PECs in the pathogenesis of podocytopathy based on currently available information.

Recurrent hypoglycemia increases hepatic gluconeogenesis without affecting glycogen metabolism or systemic lipolysis in rat.

INTRODUCTION: Recurrent hypoglycemia (RH) impairs secretion of counterregulatory hormones. Whether and how RH affects responses within metabolically important peripheral organs to counterregulatory hormones are poorly understood. OBJECTIVE: To study the effects of RH on metabolic pathways associated with glucose counterregulation within liver, white adipose tissue and skeletal muscle. METHODS: Using a widely adopted rodent model of 3-day recurrent hypoglycemia, we first checked expression of counterregulatory hormone G-protein coupled receptors (GPCRs), their inhibitory regulators and downstream enzymes catalyzing glycogen metabolism, gluconeogenesis and lipolysis by qPCR and western blot. Then, we examined epinephrine-induced phosphorylation of PKA substrates to validate adrenergic sensitivity in each organ. Next, we measured hepatic and skeletal glycogen content, degree of breakdown by epinephrine and abundance of phosphorylated glycogen phosphorylase under hypoglycemia and that of phosphorylated glycogen synthase during recovery to evaluate glycogen turnover. Further, we performed pyruvate and lactate tolerance tests to assess gluconeogenesis. Additionally, we measured circulating FFA and glycerol to check lipolysis. The abovementioned studies were repeated in streptozotocin-induced diabetic rat model. Finally, we conducted epinephrine tolerance test to investigate systemic glycemic excursions to counterregulatory hormones. Saline-injected rats served as controls. RESULTS: RH increased counterregulatory hormone GPCR signaling in liver and epidydimal white adipose tissue (eWAT), but not in skeletal muscle. For glycogen metabolism, RH did not affect total content or epinephrine-stimulated breakdown in liver and skeletal muscle. Although RH decreased expression of phosphorylated glycogen synthase 2, it did not affect hepatic glycogen biosynthesis during recovery from hypoglycemia or after fasting-refeeding. For gluconeogenesis, RH upregulated fructose 1,6-bisphosphatase 1 and monocarboxylic acid transporter 1 that imports lactate as precursor, resulting in a lower blood lactate profile during hypoglycemia. In agreement, RH elevated fasting blood glucose and caused higher glycemic excursions during pyruvate tolerance test. For lipolysis, RH did not affect circulating levels of FFA and glycerol after overnight fasting or upon epinephrine stimulation. Interestingly, RH upregulated the trophic fatty acid transporter FATP1 and glucose transporter GLUT4 to increase lipogenesis in eWAT. These aforementioned changes of gluconeogenesis, lipolysis and lipogenesis were validated in streptozotocin-diabetic rats. Finally, RH increased insulin sensitivity to accelerate glucose disposal, which was attributable to upregulated visceral adipose GLUT4. CONCLUSIONS: RH caused metabolic adaptations related to counterregulation within peripheral organs. Specifically, adrenergic signaling was enhanced in liver and visceral fat, but not in skeletal muscle. Glycogen metabolism remained unchanged. Hepatic gluconeogenesis was augmented. Systemic lipolysis was unaffected, but visceral lipogenesis was enhanced. Insulin sensitivity was increased. These findings provided insights into mechanisms underlying clinical problems associated with intensive insulin therapy, such as high gluconeogenic flux and body weight gain.

Metformin improves renal injury of MRL/lpr lupus-prone mice via the AMPK/STAT3 pathway.

OBJECTIVE: Lupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation. METHODS: In vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis. RESULTS: We found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1ß (interleukin 1ß) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro. CONCLUSIONS: Metformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway.

Thermal Properties and Key Groups Evolution of Low-Temperature Oxidation for Bituminous Coal under Lean-Oxygen Environment.

To deeply explore the spontaneous combustion disaster of coal caused by air leakage and oxygen supply, low-temperature coal oxidation experiments under different oxygen concentrations (DOC) were carried out. Within the coal spontaneous combustion characteristic measurement system, a synchronous thermal analyzer (STA) and a Fourier transform infrared spectrometer (FTIR), the macro laws of gas and heat generation under DOC are analyzed, and the mechanism of the development of coal spontaneous combustion restricted by the lean-oxygen environment is also revealed. The results show that the change of oxygen concentration (OC) does not affect the critical temperature value and gas index change trend, but the lean-oxygen environment reduces the gas concentration and heat production rate very obviously. According to the temperature of the intersection, OC needs to be lowered to less than 5% when preventing spontaneous combustion of coal. The chain thermal reaction lags in the lean-oxygen environment, and the pyrolysis activity is significantly reduced. Meanwhile, the temperature points at T 6 and T 7 show significant differences. Furthermore, with increasing OC and temperature, the content of the aliphatic hydrocarbon presents an overall trend of first increasing, then decreasing, and continuously increasing after stage IV. It is concluded that •OH, aliphatic hydrocarbons, aromatic hydrocarbons, and carboxyl groups are the key groups for the coal spontaneous combustion evolution under DOC. To combine the spontaneous combustion reaction of coal in the DOC environment, the reaction path of the index gas in the macroscopic phenomenon and the reason for the concentration differences are revealed, the mechanism for exotherm varies caused by OC is clarified, and the microscopic inhibition affection on the chain reaction within the lean-oxygen environment is also explored. The results put forward the key groups evolution mechanism under the DOC for coal oxidation, which could provide the technical guidance for the fire prevention and control on coal mines.

Effect of the reignition characteristics on long-flame coal by oxidization and water immersion.

After a coal seam is mined, the coal remaining in the goaf is prone to flooding and spontaneous combustion accidents. To explore the reignition (secondary oxidation) characteristics of long-flame coal after oxidation and water immersion, the experimental methods of thermogravimetric analysis and infrared spectroscopy were used to analyze coal samples of oxidation first and then water immersion (FO) and samples of water immersion first and then oxidization (FI) at different pre-oxidation temperatures. The results showed that the content of main oxygen-containing functional groups (hydroxyl, carbonyl, and carboxyl groups) of the FO120 (oxidation 120 °C first and then water immersion) coal sample increased, and the FI 90 (water immersion first and then oxidization 90 °C) coal sample decreased. Pre-oxidation at 120 °C will slow down the decrease in the extent of low-temperature secondary oxidation TG, as the pre-oxidation temperature increases, the total heat release of the FO coal samples first increase and then decrease, and the heat released is high at 120 °C. The FI coal samples transfer active sites during the water immersion process, and the high pre-oxidation temperature leads to the rapid increase of the speed of the primary active site, which leads to the transformation between the secondary active site and the oxygen-containing group, resulting in the cleavage of the oxygen-containing group and increasing the heat production. Water immersion pre-oxidation performed under different conditions has the dual effects of promoting and inhibiting spontaneous coal combustion. This result provides a theoretical basis for preventing spontaneous combustion in coal-mined areas in shallow coal seams after soaking in water.

Relationship between lysosomal dyshomeostasis and progression of diabetic kidney disease.

Lysosomes are organelles involved in cell metabolism, waste degradation, and cellular material circulation. They play a key role in the maintenance of cellular physiological homeostasis. Compared with the lysosomal content of other organs, that of the kidney is abundant, and lysosomal abnormalities are associated with the occurrence and development of certain renal diseases. Lysosomal structure and function in intrinsic renal cells are impaired in diabetic kidney disease (DKD). Promoting lysosomal biosynthesis and/or restoring lysosomal function can repair damaged podocytes and proximal tubular epithelial cells, and delay the progression of DKD. Lysosomal homeostasis maintenance may be advantageous in alleviating DKD. Here, we systematically reviewed the latest advances in the relationship between lysosomal dyshomeostasis and progression of DKD based on recent literature to further elucidate the mechanism of renal injury in diabetes mellitus and to highlight the application potential of lysosomal homeostasis maintenance as a new prevention and treatment strategy for DKD. However, research on screening effective interventions for lysosomal dyshomeostasis is still in its infancy, and thus should be the focus of future research studies. The screening out of cell-specific lysosomal function regulation targets according to the different stages of DKD, so as to realize the controllable targeted regulation of cell lysosomal function during DKD, is the key to the successful clinical development of this therapeutic strategy.

Importance of urinary mitochondrial DNA in diagnosis and prognosis of kidney diseases.

Mitochondrial injury plays an important role in the occurrence and development of kidney diseases. However, the existing assays to determine mitochondrial function restrict our ability to understand the relationship between mitochondrial dysfunction and kidney damage. These limitations may be overcome by recent findings on urinary mitochondrial DNA (UmtDNA). Elevated UmtDNA level may serve as a surrogate biomarker of mitochondrial dysfunction, kidney damage, and progression and prognosis of kidney diseases. Herein, we review the recent research progress on UmtDNA in kidney diseases diagnosis and highlight the research areas that should be expanded in future as well as discuss the future perspectives.

Emerging role of transcription factor EB in mitochondrial quality control.

Mitochondria are energy producers that play a vital role in cell survival. Mitochondrial dysfunction is involved in many diseases, including metabolic syndrome, neurodegenerative disorders, cardiomyopathies, cancer, obesity, and diabetic kidney disease, and challenges still remain in terms of treatments for these diseases. Mitochondrial quality control (MQC), which is defined as the maintenance of the quantity, morphology, and function of mitochondria, plays a pivotal role in maintaining cellular metabolic homeostasis and cell survival. Recently, growing evidence suggests that the transcription factor EB (TFEB) plays a pivotal role in MQC. Here, we systemically investigate the potential role and mechanisms of TFEB in MQC, which include the activation of mitophagy, regulation of mitochondrial biogenesis, reactive oxygen species (ROS) clearance, and the balance of mitochondria fission-fusion cycle. Importantly, we further discuss the therapeutic measures and effects aimed at TFEB on mitochondrial dysfunction-related diseases. Taken together, targeting TFEB to regulate MQC may represent an appealing therapeutic strategy for mitochondrial dysfunction related-diseases.