Different fates of Sb(III) and Sb(V) during the formation of jarosite mediated by Acidithiobacillus ferrooxidans.

Secondary iron-sulfate minerals such as jarosite, which are easily formed in acid mine drainage, play an important role in controlling metal mobility. In this work, the typical iron-oxidizing bacterium Acidithiobacillus ferrooxidans ATCC 23270 was selected to synthesize jarosite in the presence of antimony ions, during which the solution behavior, synthetic product composition, and bacterial metabolism were studied. The results show that in the presence of Sb(V), Fe2+ was rapidly oxidized to Fe3+ by A. ferrooxidans and Sb(V) had no obvious effect on the biooxidation of Fe2+ under the current experimental conditions. The presence of Sb(III) inhibited bacterial growth and Fe2+ oxidation. For the group with Sb(III), products with amorphous phases were formed 72 hr later, which were mainly ferrous sulfate and pentavalent antimony oxide, and the amorphous precursor was finally transformed into a more stable crystal phase. For the group with Sb(V), the morphology and structure of jarosite were changed in comparison with those without Sb. The biomineralization process was accompanied by the removal of 94% Sb(V) to form jarosite containing the Fe-Sb-O complex. Comparative transcriptome analysis shows differential effects of Sb(III) and Sb(V) on bacterial metabolism. The expression levels of functional genes related to cell components were much more downregulated for the group with Sb(III) but much more regulated for that with Sb(V). Notably, cytochrome c and nitrogen fixation-relevant genes for the A.f_Fe2+_Sb(III) group were enhanced significantly, indicating their role in Sb(III) resistance. This study is of great value for the development of antimony pollution control and remediation technology.

DKK1-SE recruits AP1 to activate the target gene DKK1 thereby promoting pancreatic cancer progression.

Super-enhancers are a class of DNA cis-regulatory elements that can regulate cell identity, cell fate, stem cell pluripotency, and even tumorigenesis. Increasing evidence shows that epigenetic modifications play an important role in the pathogenesis of various types of cancer. However, the current research is far from enough to reveal the complex mechanism behind it. This study found a super-enhancer enriched with abnormally active histone modifications in pancreatic ductal adenocarcinoma (PDAC), called DKK1-super-enhancer (DKK1-SE). The major active component of DKK1-SE is component enhancer e1. Mechanistically, AP1 induces chromatin remodeling in component enhancer e1 and activates the transcriptional activity of DKK1. Moreover, DKK1 was closely related to the malignant clinical features of PDAC. Deletion or knockdown of DKK1-SE significantly inhibited the proliferation, colony formation, motility, migration, and invasion of PDAC cells in vitro, and these phenomena were partly mitigated upon rescuing DKK1 expression. In vivo, DKK1-SE deficiency not only inhibited tumor proliferation but also reduced the complexity of the tumor microenvironment. This study identifies that DKK1-SE drives DKK1 expression by recruiting AP1 transcription factors, exerting oncogenic effects in PDAC, and enhancing the complexity of the tumor microenvironment.

Ghrelin induced by ultraviolet B exposure promotes the restoration of diabetic cutaneous wound healing.

BACKGROUND: Diabetes mellitus (DM) presents impediment to wound healing. While ultraviolet B (UVB) exposure showed therapeutic potential in various skin conditions, its capacity to mediate diabetic wound healing remains unclear. To investigate the efficacy of UVB on wound healing and its underlying basis. MATERIALS AND METHODS: Male C57BL/6 mice were subjected to the high-fat diet followed by streptozotocin administration to establish the diabetic model. Upon confirmation of diabetes, full-thickness wounds were inflicted and the treatment group received UVB radiation at 50 mJ/cm2 for 5 min every alternate day for 2 weeks. Wound healing rate was then assessed, accompanied by evaluations of blood glucose, lipid profiles, CD31 expression, and concentrations of ghrelin and leptin. Concurrently, in vitro studies were executed to evaluate the protective role of ghrelin on human umbilical vein endothelial cells (HUVEC) under high glucose (HG) conditions. RESULTS: Post UVB exposure, there was a marked acceleration in wound healing in DM mice without alterations in hyperglycemia and lipid profiles. Compared to non-UVB-exposed mice, the UVB group showed enhanced angiogenesis manifested by a surge in CD31 expression. This trend appeared to be in harmony with the elevated ghrelin levels. In vitro experiments indicated that ghrelin significantly enhanced the migratory pace and angiogenic properties of HUVEC under HG-induced stress, potentially mediated by an upregulation in vascular endothelial growth factor expression. CONCLUSION: UVB exposure bolstered wound healing in diabetic mice, plausibly mediated through augmented angiogenesis induced by ghrelin secretion. Such findings underscore the vast potential of UVB-induced ghrelin in therapeutic strategies targeting diabetic wound healing.

Thermal Exfoliation and Phosphorus Doping in Graphitic Carbon Nitride for Efficient Photocatalytic Hydrogen Production.

Photocatalytic H2 evolution has been regarded as a promising technology to alleviate the energy crisis. Designing graphitic carbon nitride materials with a large surface area, short diffusion paths for electrons, and more exposed reactive sites are beneficial for hydrogen evolution. In this study, a facile method was proposed to dope P into a graphitic carbon nitride framework by calcining melamine with 2-aminoethylphosphonic acid. Meanwhile, PCN nanosheets (PCNSs) were obtained through a thermal exfoliation strategy. Under visible light, the PCNS sample displayed a hydrogen evolution rate of 700 µmol·g-1·h-1, which was 43.8-fold higher than that of pure g-C3N4. In addition, the PCNS photocatalyst also displayed good photostability for four consecutive cycles, with a total reaction time of 12 h. Its outstanding photocatalytic performance was attributed to the higher surface area exposing more reactive sites and the enlarged band edge for photoreduction potentials. This work provides a facile strategy to regulate catalytic structures, which may attract great research interest in the field of catalysis.

Soluble RAGE attenuates myocardial I/R injury by suppressing interleukin-6.

BACKGROUND: Inflammatory responses play a central role in myocardial ischemia/reperfusion (I/R) injury. Previous studies have demonstrated that the receptor for advanced glycation end-products (RAGE) is involved in the pro-inflammatory process of myocardial I/R injury by binding to diverse ligands. Thus, the inhibitory effects of soluble receptor for advanced glycation end-products (sRAGE), a decoy receptor for RAGE, on myocardial I/R injury may be associated with a reduced inflammatory state. METHODS: In this study, plasma levels of several inflammatory mediators were measured in patients with acute myocardial infarction (AMI) and I/R-treated cardiomyocyte-specific sRAGE knock-in (sRAGE-CKI) mice. Cardiac function, infarct size, and macrophage phenotypes were examined and documented in mouse hearts. RESULTS: We enrolled 38 patients diagnosed with myocardial infarction (AMI) [mean age, 58.81 ±â€…10.40 years] and 26 control with negative coronary arteriographic findings [mean age, 61.84 ±â€…8.57 years]. The results showed that sRAGE levels were significantly elevated in the AMI patient group compared with the control group (1905.00 [1462.50, 2332.5] vs 1570.00 [1335.00, 1800.00] pg/mL, p < 0.05), which were negatively correlated with interleukin (IL)-1, IL-6, and IL-8 levels. Cardiac-specific overexpression of sRAGE dramatically improved cardiac function and reduced infarct size during myocardial I/R. Furthermore, sRAGE overexpression decreased the plasma IL-6 levels and pro-inflammatory iNOS+ M1-macrophages, and increased CD206+ M2-macrophages in the mouse hearts. CONCLUSIONS: Our findings suggested that sRAGE protects the heart from myocardial I/R injury by inhibiting the infiltration of pro-inflammatory M1-macrophages, and subsequently decreasing IL-6 secretion.

Clinical and radiological features of a cluster of immunocompetent adolescents with varicella pneumonia: a descriptive study.

Background: Varicella pneumonia is one of the most common and severe complications of chickenpox infection. This study aimed to describe the clinical and radiological features of varicella pneumonia in a cluster of immunocompetent adolescents. Methods: A retrospective analysis was conducted on a cohort of adolescent patients diagnosed with varicella pneumonia at Wuhan Jinyintan Hospital between February 2023 and May 2023. The clinical and imaging data were collected and analyzed. A total of 116 patients were divided into two groups by the absence (group 1, n=57) or presence (group 2, n=59) of lower respiratory symptoms for data comparison. Results: Among 116 patients (median age, 16 years; 60 males), rash (100%) was the most prevalent clinical symptom. The most common respiratory symptom and sign were fever (42.2%) and coarse breath sounds (41.4%). Chest computed tomography (CT) performed within five days of symptoms onset revealed multiple (89.7%), peripheral (51.7%), and ill-defined (73.3%) lung nodules in most patients, which gradually improved 6-10 days after symptom onset. Group 2 had higher levels of interleukin-6 (P<0.001), C-reactive protein (P=0.02), serum amyloid-A protein (P=0.002), longer hospital stays (P=0.04), more involved lung lobes (P=0.02), and a higher incidence of multiple nodules (P=0.043) than those of group 1. Conclusions: In immunocompetent adolescents, clustered varicella pneumonia often presents as mild and more uniform in clinical and radiological presentations than sporadic cases. The most common CT findings were multiple pulmonary nodules. Patients with lower respiratory symptoms exhibited more severe clinical and radiological manifestations. Generally, it is not recommended that patients undergo frequent CT scans in a short period.

TGM1/3-mediated transamidation of Exo70 promotes tumor metastasis upon LKB1 inactivation.

Exo70, a key exocyst complex component, is crucial for cell motility and extracellular matrix (ECM) remodeling in cancer metastasis. Despite its potential as a drug target, Exo70's post-translational modifications (PTMs) are poorly characterized. Here, we report that Exo70 is transamidated on Gln5 with Lys56 of cystatin A by transglutaminases TGM1 and TGM3, promoting tumor metastasis. This modification enhances Exo70's association with other exocyst subunits, essential for secreting matrix metalloproteinases, forming invadopodia, and delivering integrins to the leading edge. Tumor suppressor liver kinase B1 (LKB1), whose inactivation accelerates metastasis, phosphorylates TGM1 and TGM3 at Thr386 and Thr282, respectively, to inhibit their interaction with Exo70 and the following transamidation. Cantharidin, a US Food and Drug Administration (FDA)-approved drug, inhibits Exo70 transamidation to restrain tumor cell migration and invasion. Together, our findings highlight Exo70 transamidation as a key molecular mechanism and target and propose cantharidin as a therapeutic strategy with direct clinical translational value for metastatic cancers, especially those with LKB1 loss.

Commensal microbe regulation of skin cells in disease.

Human skin is the host to various commensal microbes that constitute a substantial microbial community. The reciprocal communication between these microbial inhabitants and host cells upholds both the morphological and functional attributes of the skin layers, contributing indispensably to microenvironmental and tissue homeostasis. Thus, disruption of the skin barrier or imbalances in the microbial communities can exert profound effects on the behavior of host cells. This influence, mediated by the microbes themselves or their metabolites, manifests in diverse outcomes. In this review, we examine existing knowledge to provide insight into the nuanced behavior exhibited by the microbiota on skin cells in health and disease states. These interactions provide insight into potential cellular targets for future microbiota-based therapies to prevent and treat skin disease.

The molecular and network mechanisms of antilipidemic potential effects of Ganfule capsules in nonalcoholic fatty liver disease.

Background: Non-alcoholic fatty liver disease (NAFLD) is a common liver disorder characterized by hepatic steatosis, inflammation and fibrosis. Ganfule (GFL), a traditional Chinese medicine, has demonstrated therapeutic potential in the treatment of NAFLD but the mechanisms involved are not fully understood.To evaluate the biochemical mechanisms of GFL in treating NAFLD by examining its effects on biological networks, key therapeutic targets, histopathological changes and clinical implications. Methods: Chemical component screening, key target prediction, biological functional enrichment analysis, lipid profile localization analysis and complex network analysis were performed on GFL using multi-database mining, network analysis and molecular docking. An NAFLD rat model was then established and treated with different doses of GFL. Histopathological evaluation and western blotting were used to verify the expression levels of key target proteins in GFL-treated NAFLD rats. Results: Network analysis analysis identified 12 core targets, 12 core active ingredients and 7 core Chinese medicinal herbs in GFL potentially involved in the treatment of NAFLD. Biological functional enrichment analysis revealed the involvement of lipid metabolism, apoptosis and intracellular signaling pathways. Molecular docking confirmed a strong affinity between GFL's core compounds and certain target proteins. Histopathological examination of an NAFLD rat model showed reduced hepatocellular steatosis after GFL treatment. Western blotting revealed significant downregulation of PPARA and PPARD protein expression and upregulation of PIK3CG and PRKACA protein expression in NAFLD rats treated with lower doses of GFL. Conclusions: Our results suggest that GFL modulates key proteins involved in lipid metabolism and apoptosis pathways. GFL improved the histopathological features of NAFLD rats by regulating lipid metabolism as well as reducing hepatocyte apoptosis and hepatocellular steatosis. These findings offer insights into the biochemical mechanism of action of GFL and support its use in the treatment for NAFLD.

Effect of probiotics at different intervention time on glycemic control in patients with type 2 diabetes mellitus: a systematic review and meta-analysis.

Background: Type 2 diabetes mellitus(T2DM) is characterized by hyperglycemia. Gut microbiome adjustment plays a positive part in glucose regulation, which has become a hotspot. Probiotics have been studied for their potential to control the gut flora and to treat T2DM. However, the conclusion of its glucose-lowering effect is inconsistent based on different probiotic intervention times. Objectives: To comprehensively evaluate how various probiotic intervention times affect glycemic control in people with T2DM. Methods: We retrieved PubMed, Embase, Web of Science, and Cochrane Library on randomized controlled trials(RCTs)regarding the impact of probiotics on glycemic control in patients with T2DM from the inception to November 16, 2023. Separately, two researchers conducted a literature analysis, data extraction, and bias risk assessment of the involved studies. We followed the PRISMA guidelines, used RevMan 5.4 software for meta-analysis, and assessed the risk of bias by applying the Cochrane Handbook for Systematic Reviews 5.1.0. Results: We included eight RCTs with 507 patients. Meta-analysis revealed that the use of probiotics might considerably reduce levels of glycosylated hemoglobin (HbA1c) {mean deviation (MD) = -0.33, 95% confidence interval (CI) (-0.59, -0.07), p = 0.01}, Insulin {standard mean deviation (SMD) = -0.48, 95% CI (-0.74, -0.22), p = 0.0003} and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR){SMD = -1.36, 95% CI (-2.30, -0.41), p = 0.005} than placebo group. No statistically significant differences were found regarding fasting blood glucose (FBG) and body mass index (BMI) {SMD = -0.39, 95% CI (-0.83, 0.05), p = 0.08}, {SMD = -0.40, 95% CI (-1.07, 0.27), p = 0.25}, respectively. Subgroup analyses, grouped by intervention times, showed that six to eight weeks of intervention improved HbA1c compared to the control group (p < 0.05), both six to eight weeks and 12-24 weeks had a better intervention effect on Insulin, and HOMA-IR (p < 0.05).In contrast, there was no statistically significant variation in the length between FBG and BMI regarding duration. Conclusion: This meta-analysis found probiotics at different intervention times play a positive role in modulating glucose in T2DM, specifically for HbA1c in six to eight weeks, Insulin and HOMA-IR in six to eight weeks, and 12-24 weeks. To confirm our findings, further excellent large-sample research is still required. Systematic review registration: https://www.crd.york.ac.uk/prospero, identifier CRD42023483325.

Acute changes in hippocampal metabolism after anesthesia and surgery: Implications for perioperative neurocognitive disorder.

BACKGROUND: The risk of developing dementia is higher in individuals who suffer from perioperative neurocognitive disorder (PND), including postoperative cognitive dysfunction (POCD) and delirium. Recent studies have indicated correlations between anesthesia, surgery and PND. Acute metabolic changes induced by anesthesia and surgery may be related to cognitive impairments. Despite a paucity of research on acute metabolic changes in the hippocampus during surgery, there are conflicting about specific metabolites. METHODS: We developed a mouse model of cognitive impairment induced by isoflurane anesthesia and unilateral nephrectomy. Cognition was evaluated by Y maze and fear conditioning test (FCT). The hippocampus was harvested after the surgery. LC-MS (liquid chromatography-mass spectrometry) was performed. The differential metabolites involved in lipid, amino acid, nucleotide, carbohydrate metabolism were analyzed. RESULTS: Anesthesia and surgery exposure induced cognition decline. A total of 49 metabolites were significantly up-regulated and 122 down-regulated. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway of the metabolites identified purine, glutathione, nicotinate and nicotinamide metabolism. Metabolites involved in lipid, amino acid, nucleotide, carbohydrate metabolism were identified including nicotinamide adenine dinucleotide (NAD), 1-Methylnicotinamide, propionic acid, histidine, adenosine, and guanosine cyclic monophosphate. Some metabolites exhibited a consistent change trend in the hippocampus of aging mice. CONCLUSIONS: The study indicates that anesthesia and surgery can induce acute alterations in hippocampal metabolomics, including metabolites involved in lipid, amino acid, nucleotide, and carbohydrate metabolism. These metabolites may play a role in modulating PND through the regulation of neuroinflammation, oxidative stress, blood-brain barrier (BBB) permeability.

Comprehensive proteomic characterization of urethral stricture disease in the Chinese population.

Background: Male urethral stricture disease (USD) is predominantly characterized by scar formation. There are few effective therapeutic drugs, and comprehensive molecular characterizations of USD formation remain undefined. Methods: The proteomic profiling of twelve scar tissues and five matched normal adjacent tissues (NATs). Proteomic analysis methods were applied to explore the molecular characterizations of USD formation, including uncovering mechanistic pathways and providing novel biomarkers for scar formation. Results: Comparative proteomic analysis showed that the extracellular matrix (ECM) and complement cascade signaling were predominant in scar tissues. COL11A1 and CD248 significantly contributed to the accumulation of ECM components. Our study presented diverse molecular mechanisms of scar formation across different ages and suggested the potential effects of PXK in Age 1 (<45) patients. Furthermore, immune infiltration studies indicated the therapeutic potential of inhibiting the complement system (C4A, C4B) in Age 2 (≥45) patients, providing a potential clinical strategy for USD. Conclusion: This study illustrated the pathogenesis of USD formation and the diverse characteristics of USD patients with different ages, enhancing our understanding of the disease's pathogenesis and providing a valuable resource for USD treatment.

Enhanced atherosclerosis in apolipoprotein E knockout rabbits: role of apoB48-rich remnant lipoproteins.

Introduction: Apolipoprotein E (apoE) acts as a binding molecule for both the low-density lipoprotein receptor and the lipoprotein receptor-related protein and this function is essential for facilitating the hepatocyte uptake of lipoproteins containing apoB. The absence of apoE leads to increased atherogenicity in both humans and mice, although the precise molecular mechanisms remain incompletely understood. Objectives: This study aimed to investigate the susceptibility of apoE knockout (KO) rabbits, in comparison with wild-type (WT) rabbits, to diet-induced hyperlipidemia and atherosclerosis. Methods: ApoE KO rabbits and WT rabbits were fed a diet containing 0.3% cholesterol for 16 weeks. Plasma lipid levels, lipoproteins, and apolipoproteins were analyzed. Atherosclerosis was evaluated at the endpoint of experiments. In addition, we evaluated the oxidizability of those lipoproteins containing apoB to investigate the possible mechanisms of atherosclerosis. Results: Male apoE KO rabbits showed significantly elevated levels of total cholesterol and triglycerides compared to WT rabbits, while female apoE KO rabbits displayed similar high total cholesterol levels, albeit with significantly higher triglycerides levels than WT controls. Notably, both male (2.1-fold increase) and female (1.6-fold increase) apoE KO rabbits exhibited a significantly augmented aortic lesion area compared to WT controls. Pathological examination showed that the increased intimal lesions in apoE KO rabbits were featured by heightened infiltration of macrophages (2.7-fold increase) and smooth muscle cells (2.5-fold increase). Furthermore, coronary atherosclerotic lesions were also increased by 1.3-fold in apoE KO rabbits. Lipoprotein analysis revealed that apoB48-rich beta-very-low-density lipoproteins were notably abundant in apoE KO rabbits, suggesting that these remnant lipoproteins of intestinal origin serve as the primary atherogenic lipoproteins. Moreover, apoB48-rich remnant lipoproteins isolated from apoE KO rabbits exhibited heightened susceptibility to copper-induced oxidation. Conclusions: The findings indicate that apoB48-rich remnant lipoproteins, resulting from apoE deficiency, possess greater atherogenic potential than apoB100-rich remnant lipoproteins, regardless of plasma TC levels.

Molecular mechanism of regulating tat protein expression of pingganjiedu TCM in the treatment of AIDS based on network pharmacology.

AIDS is a serious disease with impaired immune function caused by human immunodeficiency virus (HIV) infection. The treatment of AIDS has always been the focus of global scientific research, and Tat protein is a key regulatory protein in the process of HIV infection. Its high expression is closely related to virus replication, disease progression, etc. The aim of this study is to explore the molecular mechanism of regulating Tat protein expression by using network pharmacology based traditional Chinese medicine for calming the liver and detoxifying. 129 AIDS patients were enrolled in the study and randomly divided into HAART combined with PGJDP treatment and HAART alone treatment groups. The virological response rate, immunological response status (CD4 + T cell level, CD4/CD8) and incidence of abnormal liver function were observed before and 48 weeks after treatment. Using the TCMSP database to obtain the chemical components and targets of the main traditional Chinese medicine components in PGJDP, clinical results indicate that the combination of HAART and PGJDP treatment can improve the virological response rate (P > 0.05); Increase the number of CD4 + T lymphocytes (P > 0.05); Significantly increased CD4/CD8 ratio (P < 0.01); Simultaneously, it significantly reduced the incidence of liver dysfunction (P < 0.01). After screening and analysis, the Chinese herbal medicine for calming liver and detoxifying has the potential to significantly regulate the expression of Tat protein. These Chinese herbal compounds can reduce the expression of Tat protein by affecting key pathways and regulating the expression of related genes, which has potential therapeutic effects on the treatment of AIDS.

Exosomes-mediated retinoic acid disruption: A link between gut microbiota depletion and impaired spermatogenesis.

Gut microbiota symbiosis faces enormous challenge with increasing exposure to drugs such as environmental poisons and antibiotics. The gut microbiota is an important component of the host microbiota and has been proven to be involved in regulating spermatogenesis, but the molecular mechanism is still unclear. A male mouse model with gut microbiota depletion/dysbiosis was constructed by adding combined antibiotics to free drinking water, and reproductive parameters such as epididymal sperm count, testicular weight and paraffin sections were measured. Testicular transcriptomic and serum metabolomic analyses were performed to reveal the molecular mechanism of reproductive dysfunction induced by gut microbiota dysbiosis in male mice.This study confirms that antibiotic induced depletion of gut microbiota reduces sperm count in the epididymis and reduces germ cells in the seminiferous tubules in male mice. Further study showed that exosomes isolated from microbiota-depleted mice led to abnormally high levels of retinoic acid and decrease in the number of germ cells in the seminiferous tubules and sperm in the epididymis. Finally, abnormally high levels of retinoic acid was confirmed to disrupted meiotic processes, resulting in spermatogenesis disorders. This study proposed the concept of the gut microbiota-exosome-retinoic acid-testicular axis and demonstrated that depletion of the gut microbiota caused changes in the function of exosomes, which led to abnormal retinoic acid metabolism in the testis, thereby impairing meiosis and spermatogenesis processes.

Soluble receptor for advanced glycation end-products positively correlated to kidney injury with coronary heart disease.

AIMS: Coronary heart disease (CHD) patients with changed serum soluble receptor for advanced glycation end products (sRAGE) will experience microalbuminuria and even kidney dysfunction. However, the role of sRAGE for microalbuminuria in CHD is still not established. This study aimed to evaluate the association between sRAGE and early kidney dysfunction in CHD patients. MATERIALS AND METHODS: In this cross-sectional study, sRAGE and urinary albumin-to-creatinine ratio (uACR) were measured in hospitalized CHD patients who have undergone coronary arteriography to evaluate the distinction and correlation between sRAGE and uACR. RESULTS: There were 127 CHD patients (mean age: 63.06 ±â€¯10.93 years, 93 males) in the study, whose sRAGE were 1.83 ±â€¯0.64 µg/L. The sRAGE level was higher in kidney injury group (uACR ≥ 30 mg/g) compared with no kidney injury group (uACR < 30 mg/g) [(2.08 ±â€¯0.70 vs. 1.75 ±â€¯0.61) µg/L, P < 0.05]. Moreover, the positive correlation between serum sRAGE and uACR was significant in CHD patients (r = 0.196, P < 0.05). Binary logistic regression suggests sRAGE as a predictor for microalbuminuria in CHD patients [Odd Ratio = 2.62 (1.12-6.15), P < 0.05)]. The area under the receiver operating characteristic curve (AUC) of sRAGE is higher than that of the traditional indicators of renal function such as creatinine and estimated glomerular filtration rate, indicating sRAGE might have a good performance in evaluating early kidney injury in CHD patients [AUC is 0.660 (0.543-0.778), P < 0.01)]. CONCLUSIONS: Serum sRAGE was positively correlated to uACR and might serve as a potential marker to predict early kidney injury in CHD patients.

Detecting Transitions from Stability to Instability in Robotic Grasping Based on Tactile Perception.

Robots execute diverse load operations, including carrying, lifting, tilting, and moving objects, involving load changes or transfers. This dynamic process can result in the shift of interactive operations from stability to instability. In this paper, we respond to these dynamic changes by utilizing tactile images captured from tactile sensors during interactions, conducting a study on the dynamic stability and instability in operations, and propose a real-time dynamic state sensing network by integrating convolutional neural networks (CNNs) for spatial feature extraction and long short-term memory (LSTM) networks to capture temporal information. We collect a dataset capturing the entire transition from stable to unstable states during interaction. Employing a sliding window, we sample consecutive frames from the collected dataset and feed them into the network for the state change predictions of robots. The network achieves both real-time temporal sequence prediction at 31.84 ms per inference step and an average classification accuracy of 98.90%. Our experiments demonstrate the network's robustness, maintaining high accuracy even with previously unseen objects.

Negatively Charged Carbon Dots Employed Symplastic and Apoplastic Pathways to Enable Better Plant Delivery than Positively Charged Carbon Dots.

Efficient delivery of nanoparticles (NPs) to plants is important for agricultural application. However, to date, we still lack knowledge about how NPs' charge matters for its translocation pathway, i.e., symplastic and apoplastic pathways, in plants. In this study, we synthesized and used negatively charged citrate sourced carbon dots (C-CDs, -37.97 ± 1.89 mV), Cy5 coated C-CDs (Cy5-C-CDs, -41.90 ± 2.55 mV), positively charged PEI coated carbon dots (P-CDs, +43.03 ± 1.71 mV), and Cy5 coated P-CDs (Cy5-P-CDs, +48.80 ± 1.21 mV) to investigate the role of surface charges and coatings on the employed translocation pathways (symplastic and apoplastic pathways) of charged NPs in plants. Our results showed that, different from the higher fluorescence intensity of P-CDs and Cy5-P-CDs in extracellular than intracellular space, the fluorescence intensity of C-CDs and Cy5-C-CDs was similar between intracellular and extracellular space in cucumber and cotton roots. It suggests that the negatively charged CDs were translocated via both symplastic and apoplastic pathways, but the positively charged CDs were mainly translocated via the apoplastic pathway. Furthermore, our results showed that root applied negatively charged C-CDs demonstrated higher leaf fluorescence than did positively charged P-CDs in both cucumber (8.09 ± 0.99 vs 3.75 ± 0.23) and cotton (7.27 ± 1.06 vs 3.23 ± 0.22), indicating that negatively charged CDs have a higher translocation efficiency from root to leaf than do positively charged CDs. It should be noted that CDs do not affect root cell activities, ROS level, and photosynthetic performance in cucumber and cotton, showing its good biocompatibility. Overall, this study not only figured out that root applied negatively charged CDs employed both symplastic and apoplastic pathways to do the transportation in roots compared with mainly the employment of apoplastic pathway for positively charge CDs, but also found that negatively charge CDs could be more efficiently translocated from root to leaf than positively charged CDs, indicating that imparting negative charge to NPs, at least CDs, matters for its efficient delivery in crops.

van der Waals-bonded graphene clusters enhance thermal conductivity of phase-change materials for advanced thermal energy management.

Organic phase-change materials possess immense application potential, but their low thermal conductivity (≤0.5 W m-1 K-1) severely limits the thermal energy charge/discharge rate, impeding their practical implementation in the field of advanced energy. While incorporating thermally conductive fillers into the phase-change matrix can address this issue, achieving a thermal conductivity exceeding 10 W m-1 K-1 at a filler content below 30 vol% remains challenging, attributed to the absence of a well-designed filler interface and structure. Herein, a strategy for developing planar graphene clusters and subsequently integrating them with phase-change microcapsules to fabricate composites using compression molding was demonstrated. The proposed graphene clusters are formed by closely aligned and overlapping graphene sheets that bond together through van der Waals forces, resulting in a significant decrease in junction thermal resistance within the composites. Combining this interface design with compression-induced construction of a highly oriented structure, the composites achieved a remarkable thermal conductivity of 103 W m-1 K-1 with ≈29 vol% filler addition, enhancing the thermal energy charge/discharge rate by over two orders of magnitude. Furthermore, we demonstrated that the composites possess the essential enthalpy values, competent strength, and ease of shaping, making them applicable across various domains of thermal energy management.

[Anti-myocardial ischemic injury effects and mechanisms of cryptotanshinone in regulating macrophage polarisation through Dectin-1 signalling pathway].

The aim of this study was to investigate the potential mechanism by which cryptotanshinone(CTS) may exert its anti-myo-cardial ischemic effect through the regulation of macrophage polarization via the dendritic cell-associated C-type lectin 1(Dectin-1) signaling pathway. Male C57BL/6 mice, aged six weeks, were utilized to establish myocardial ischemia models and were subsequently divided into five groups: sham, model, CTS low-dose(21 mg·kg~(-1)·d~(-1)), CTS high-dose(84 mg·kg~(-1)·d~(-1)), and dapagliflozin(0.14 mg·kg~(-1)·d~(-1)). The cardiac function, serum enzyme levels, Dectin-1 expression, macrophage polarization, and neutrophil infiltration in the myocardial infarction area were assessed in each group. An in vitro model of M1-type macrophages was constructed using lipopolysaccharide/interfe-ron-γ(LPS/IFN-γ) stimulated RAW264.7 cells to investigate the impact of CTS on macrophage polarization and to examine alterations in key proteins within the Dectin-1 signaling pathway. In the CTS group, compared to the model group mice, there was a significant improvement in the cardiac function and myocardial injury, along with a notable increase in the ratio of M2/M1-type macrophages in the myocardial infarcted area and a decrease in neutrophil infiltration. Additionally, Dectin-1 exhibited low expression. The results of in vitro experiments demonstrated that CTS can decrease the expression of M1-type marker genes and increase the expression of M2-type marker genes. Besides, it can decrease the levels of Dectin-1 and the phosphorylation of its associated proteins, including spleen tyrosine kinase(Syk), protein kinase B(Akt), nuclear factor-kappaB p65(NF-κB p65), and extracellular signal-regulated protein kinases(ERK1/2). Additionally, CTS was found to enhance the phosphorylation of signal transducer and activator of transcription-6(STAT6). The above results suggest that CTS exerts its anti-myocardial ischemic injury effect by regulating macrophage polarization through the Dectin-1 signaling pathway.