Simple synthesis of peanut shell-like MoCoFe-HO@CoMo-LDH for efficient alkaline oxygen evolution reaction.

Due to the depletion of fossil energy on earth, it is crucial to develop resource rich and efficient non-precious metal electrocatalysts for oxygen evolution reaction (OER). Herein, we synthesized an efficient and economical electrocatalyst using a simple self-assembly strategy. Firstly, rod-shaped MIL-88A was synthesized by hydrothermal method. Then, the surface of MIL-88A was functionalized and encapsulated in zeolitic imidazolate framework-67 (ZIF-67) by hydrothermal method. The combination of MIL-88A and ZIF-67 resulted in a slight ion-exchange reaction between Co2+ and the surface of MIL-88A to generate CoFe-LDH@ZIF-67 core-shell structure. Afterwards, in the presence of Mo6+, ZIF-67 was converted into CoMo-nanocages through ion-exchange reactions, forming a core-shell structure of MoCoFe hydr (oxy) oxide@CoMo-LDH (MoCoFe-HO@CoMo-LDH). Due to the advantages of core-shell structure and composition, this material exhibits excellent OER characteristics, with a small Tafel slope (45.11 mV dec-1) and low overpotential (324 mV) at 10 mA cm-2. It exhibits good stability in alkaline media. This research work provides a novel approach for the development of efficient and economical non-precious metal electrocatalysts.

Knockdown of circ-Gatad1 alleviates LPS induced HK2 cell injury via targeting miR-22-3p/TRPM7 axis in septic acute kidney.

BACKGROUND: Sepsis is a life-threatening, systemic inflammatory disease that can lead to a variety of conditions, including septic acute kidney injury (AKI). Recently, multiple circular Rnas (circRNAs) have been implicated in the development of this disease. METHODS: In this study, we aimed to elucidate the role of circ-Gatad1 in sepsis induced AKI and its potential mechanism of action. High-throughput sequencing was used to investigate abnormal expression of circRNA in AKI and healthy volunteer. Bioinformatics analysis and luciferase reporting analysis were used to clarify the interacted relationship among circRNA, miRNA and mRNA. HK2 cells were treated with lipopolysaccharide (LPS) to establish septic AKI cell model. HK2 cells were employ to analysis the ROS, inflammatory cytokines expression, proliferation and apoptosis under LPS condition. RESULTS: The result show that the expression of circ-Gatad1 was increased in septic acute kidney patients. Downregulation circ-Gatad1 suppressed LPS-treated induced HK2 cells injury including apoptosis, proliferation ability, ROS and inflammatory cytokines level. Bioinformatics and luciferase report analysis confirmed that both miR-22-3p and TRPM7 were downstream targets of circ-Gatad1. Overexpression of TRPM7 or downregulation of miR-22-3p reversed the protective effect of si-circ-Gatad1 to HK2 after exposure to LPS (5 µg/ml) microenvironment. CONCLUSION: In conclusion, knockdown of circ-Gatad1 alleviates LPS induced HK2 cell injury via targeting miR-22-3p/TRPM7 axis in septic acute kidney.

MicroRNAs Promote the Progression of Sepsis-Induced Cardiomyopathy and Neurovascular Dysfunction Through Upregulation of NF-kappaB Signaling Pathway-Associated HDAC7/ACTN4.

Introduction: The objective of this study was to determine the NF-kappaB pathway, hub genes, and transcription factors (TFs) in monocytes implicated in the progression of neurovascular-related sepsis-induced cardiomyopathy (SIC) as well as potential miRNAs with regulatory functions. Methods: : Sepsis-induced cardiomyopathy-and heart failure (HF)-related differentially expressed genes (DEGs) between SIC and HF groups were identified separately by differential analysis. In addition, DEGs and differentially expressed miRNAs (DEmiRNAs) in monocytes between sepsis and the HC group were identified. Then, common DEGs in SIC, HF, and monocyte groups were identified by intersection analysis. Based on the functional pathways enriched by these DEGs, genes related to the NF-kB-inducing kinase (NIK)/NF-kappaB signaling pathway were selected for further intersection analysis to obtain hub genes. These common DEGs, together with sepsis-related DEmiRNAs, were used to construct a molecular interplay network and to identify core TFs in the network. Results: : A total of 153 upregulated genes and 25 downregulated genes were obtained from SIC-, HF-, and monocyte-related DEGs. Functional pathway analysis revealed that the upregulated genes were enriched in NF-κB signaling pathway. A total of eight genes associated with NF-κB signaling pathway were then further identified from the 178 DEGs. In combination with sepsis-related DEmiRNAs, HDAC7/ACTN4 was identified as a key transcriptional regulatory pair in the progression of SIC and in monocyte regulation. hsa-miR-23a-3p, hsa-miR-3175, and hsa-miR-23b-3p can regulate the progression of SIC through the regulation of HDAC7/ACTN4. Finally, gene set enrichment analysis (GSEA) suggested that HDAC7/ACTN4 may be associated with apoptosis in addition to the inflammatory response. Conclusion: : hsa-miR-23a-3p, hsa-miR-3175, and hsa-miR-23b-3p are involved in SIC progression by regulating NF-κB signaling signaling pathway-related HDAC7/ACTN4 in monocytes and cardiac tissue cells. These mechanisms may contribute to sepsis-induced neurovascular damage.

Multiple organ dysfunction syndrome, an unusual complication of heroin intoxication: a case report and review of literature.

Multiple organ dysfunction syndrome (MODS) has rarely been described in patients with heroin intoxication. Here, we report a rare case of MODS involving six organs, due to heroin intoxication. The patient was a 32-year-old Chinese man with severe heroin intoxication complicated by acute pulmonary edema and respiratory insufficiency, shock, myocardial damage and cardiac insufficiency, rhabdomyolysis and acute renal insufficiency, acute liver injury and hepatic insufficiency, toxic leukoencephalopathy, and hypoglycemia. He managed to survive and was discharged after 10 weeks of intensive care. The possible pathogenesis and therapeutic measures of MODS induced by heroin intoxication and some suggestions for preventing and treating severe complications of heroin intoxication, based on clinical evidence and the pertinent literature, are discussed in this report.

Doença de Haff complicada por falência de múltiplos órgãos após ingestão de lagostim: estudo de caso / Haff disease complicated by multiple organ failure after crayfish consumption: a case study

A doença de Haff é uma síndrome que consiste de rabdomiólise não explicada. Pacientes que apresentam a doença de Haff relatam ter ingerido pescado nas últimas 24 horas antes do início da doença. A maioria dos pacientes sobrevive apresentando breve recuperação. O presente artigo é o primeiro relato de doença de Haff complicada por falência de múltiplos órgãos após ingestão de lagostim. Um homem chinês de 66 anos de idade ingeriu lagostim cozido na noite de 23 de junho de 2013. Chegou ao hospital 2 dias mais tarde, sendo admitido à unidade de terapia intensiva. Após a admissão, o paciente recebeu o diagnóstico de doença de Haff complicada por falência de múltiplos órgãos. Apesar dos tratamentos de suporte e sintomático, a condição do paciente deteriorou, vindo o mesmo a falecer em consequência da doença. A doença de Haff é uma rara síndrome clínica que é, às vezes, mal diagnosticada. O diagnóstico precoce e o tratamento adequado são essenciais para prevenir a progressão para falência de múltiplos órgãos.

Haff disease is a syndrome consisting of unexplained rhabdomyolysis. Patients suffering from Haff disease report having eaten fish within 24 hours before the onset of illness. Most patients survive and recover quickly. The present study is the first report of Haff disease complicated by multiple organ failure after crayfish consumption. A 66-year-old Chinese man ate cooked crayfish on the night of June 23, 2013. He arrived at our hospital 2 days later and was admitted to the intensive care unit. After admission, the patient was diagnosed with Haff disease complicated by multiple organ failure. Despite supportive and symptomatic treatments, the condition of the patient deteriorated, and he died due to his illness. Haff disease is a rare clinical syndrome that is sometimes misdiagnosed. Early diagnosis and proper treatment are essential to prevent progression to multiple organ failure.

Haff disease complicated by multiple organ failure after crayfish consumption: a case study.

Haff disease is a syndrome consisting of unexplained rhabdomyolysis. Patients suffering from Haff disease report having eaten fish within 24 hours before the onset of illness. Most patients survive and recover quickly. The present study is the first report of Haff disease complicated by multiple organ failure after crayfish consumption. A 66-year-old Chinese man ate cooked crayfish on the night of June 23, 2013. He arrived at our hospital 2 days later and was admitted to the intensive care unit. After admission, the patient was diagnosed with Haff disease complicated by multiple organ failure. Despite supportive and symptomatic treatments, the condition of the patient deteriorated, and he died due to his illness. Haff disease is a rare clinical syndrome that is sometimes misdiagnosed. Early diagnosis and proper treatment are essential to prevent progression to multiple organ failure.