Integrated bioinformatics and machine learning algorithms reveal the unfolded protein response pathways and immune infiltration in acute myocardial infarction.

Background: The unfolded protein response (UPR) is a critical biological process related to a variety of physiological functions and cardiac disease. However, the role of UPR-related genes in acute myocardial infarction (AMI) has not been well characterized. Therefore, this study aims to elucidate the mechanism and role of the UPR in the context of AMI.

Antimicrobial Step-Down Therapy versus Conventional Antimicrobial Therapy in the Treatment of Patients with Sepsis.

Objective: This study was to evaluate the efficacy of antimicrobial step-down therapy versus conventional antimicrobial therapy in the treatment of patients with sepsis.

Methods: Between September 2020 and September 2021, 65 patients with sepsis treated in the intensive care unit (ICU) of our hospital were recruited and assigned at a ratio of 1 : 1 to receive either conventional antimicrobial therapy (sulbactam plus cefoperazone) (control group) or antimicrobial step-down therapy (imipenem/cilastatin) (observation group). The results of drug sensitivity tests and clinical effects were evaluated comprehensively after 3-5 d of treatment, downgraded, and upgraded, or maintenance treatment was administered for 10 d.

LncRNA SNHG1 promotes sepsis-induced myocardial injury by inhibiting Bcl-2 expression via DNMT1.

Myocardial injury is a frequently occurring complication of sepsis. This study aims to investigate the molecular mechanism of long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1)-mediated DNA methyltransferase 1/B-cell lymphoma-2 (DNMT1/Bcl-2) axis in sepsis-induced myocardial injury. Mice and HL-1 cells were treated with lipopolysaccharide (LPS) to establish animal and cellular models simulating sepsis and inflammation.

CCCTC-binding factor-mediated microRNA-340-5p suppression aggravates myocardial injury in rats with severe acute pancreatitis through activation of the HMGB1/TLR4 axis.

Background: Severe acute pancreatitis (SAP) is a life-threatening disorder associated with multisystem organ failure. This study aimed to investigate the function of high mobility group box 1 (HMGB1) in SAP-induced myocardial injury.

Methods: A rat model with SAP was induced.

miR-340-5p inhibits pancreatic acinar cell inflammation and apoptosis via targeted inhibition of HMGB1.

Acute pancreatitis (AP) is a common gastrointestinal disease that affects 1 million individuals worldwide. Inflammation and apoptosis are considered to be important pathogenic mechanisms of AP, and high mobility group box 1 (HMGB1) has been shown to play a particularly important role in the etiology of this disease. MicroRNAs (miRs) are emerging as critical regulators of gene expression and, as such, they represent a promising area of therapeutic target identification and development for a variety of diseases, including AP.

Interfering hsa_circ_0073748 alleviates caerulein-induced ductal cell injury in acute pancreatitis by inhibiting miR-132-3p/TRAF3/NF-κB pathway.

Circular RNA hsa_circ_0073748 (circ_0073748) is upregulated in patients with acute pancreatitis (AP), a clinically common sudden inflammatory response. MicroRNA (miR)-132-3p is a stress-induced factor with high conservation between species. Herein, expression and role of circ_0073748 and miR-132-3p in caerulein-induced pancreatitis were studied.

MALAT1 shuttled by extracellular vesicles promotes M1 polarization of macrophages to induce acute pancreatitis via miR-181a-5p/HMGB1 axis.

Acute pancreatitis (AP) is a serious condition carrying a mortality of 25-40%. Extracellular vesicles (EVs) have reported to exert potential functions in cell-to-cell communication in diseases such as pancreatitis. Thus, we aimed at investigating the mechanisms by which EV-encapsulated metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) might mediate the M1 polarization of macrophages in AP.

C/EBP β Mediates the Aberrant Inflammatory Response and Cell Cycle Arrest in Lps-stimulated Human Renal Tubular Epithelial Cells by Regulating NF-κB Pathway.

Background And Aims: The main cause of sepsis-induced Acute kidney injury (AKI) is acute infection after surgery and subsequent progression. However, the mechanism by which AKI is caused and developed from sepsis are not completely known. Herein, we determined the role of CCAAT/enhancer-binding protein β (C/EBP β) in sepsis-induced AKI METHODS: C/EBP β expression was up or down-regulated in LPS-stimulated human renal tubular epithelial cells in vitro by recombinant adenoviruses or siRNA.

Long non-coding RNA SNHG14 aggravates LPS-induced acute kidney injury through regulating miR-495-3p/HIPK1.

Acute kidney injury (AKI) is a complex syndrome with an abrupt decrease of kidney function, which is associated with high morbidity and mortality. Sepsis is the common cause of AKI. Mounting evidence has demonstrated that long non-coding RNAs (lncRNAs) play critical roles in the development and progression of sepsis-induced AKI.

Silencing of CREB Inhibits HDAC2/TLR4/NF-κB Cascade to Relieve Severe Acute Pancreatitis-Induced Myocardial Injury.

The purpose of the present study is to investigate the role of CREB in cardiomyocytes proliferation in regulation of HDAC2-dependent TLR4/NF-κB pathway in severe acute pancreatitis (SAP)-induced myocardial injury. The SAP rat model was developed by injecting sodium touracholate into SD rats and then infected with lentivirus vectors expressing sh-CREB in the presence/absence of LPS. The pathological alterations of rat pancreatic and cardiac tissues were observed by HE staining.

miR-29a-3p transferred by mesenchymal stem cells-derived extracellular vesicles protects against myocardial injury after severe acute pancreatitis.

Aims: Acute pancreatitis (AP) is an inflammatory disease of the pancreas that may affect local tissues or remote organ systems, while severe acute pancreatitis (SAP) is a life-threatening disorder associated with multiple organ failure. In this investigation, we set about to determine whether microRNA-29a-3p (miR-29a-3p) carried by mesenchymal stem cell (MSCs)-derived extracellular vesicles (EVs) affects the myocardial injury during SAP.

Main Methods: EVs were isolated from MSCs of rat bone marrow by differential centrifugation.

Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway.

Myocardial infarction (MI) is one of the most serious cardiovascular diseases associated with myocardial ischemia/reperfusion (I/R) injury. Glaucocalyxin A (GLA) is a biologically active ent-kauranoid diterpenoid that has been found to ameliorate myocardial I/R injury in mice. However, the mechanism has not been fully investigated.

HIPK2 overexpression relieves hypoxia/reoxygenation-induced apoptosis and oxidative damage of cardiomyocytes through enhancement of the Nrf2/ARE signaling pathway.

Homeodomain interacting protein kinase-2 (HIPK2) has emerged as a crucial stress-responsive kinase that plays a critical role in regulating cell survival and apoptosis. However, whether HIPK2 participates in regulating cardiomyocyte survival during myocardial ischemia/reperfusion injury remains unclear. Here, we investigated the regulatory effect of HIPK2 on hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury and its potential underlying molecular mechanism.

Long noncoding RNA LINC00657 induced by SP1 contributes to the non-small cell lung cancer progression through targeting miR-26b-5p/COMMD8 axis.

Non-small-cell lung cancer (NSCLC) is a kind of lung cancer with high incidence and poor outcomes all over the world. Studies have validated that the upregulation of long noncoding RNA LINC00657 is related to several cancers. Nevertheless, the underlying regulatory mechanism of LINC00657 in NSCLC has not been well elucidated.

Identification of microRNAs as potential biomarkers for lung adenocarcinoma using integrating genomics analysis.

Lung adenocarcinoma (LUAD) is the most common histological subtype of non-small cell lung cancer, but novel biomarkers for early diagnosis are lacking. Extensive effort has been exerted to identify miRNA biomarkers in LUAD. Unfortunately, high inter-lab variability and small sample sizes have produced inconsistent conclusions in this field.

The role of JAK/STAT3 signaling pathway on apoptosis of lung adenocarcinoma cell line PC-9 induced by icotinib.

Objective: The aim of this study is to estimate the role of JAK/STAT3 signaling pathway on apoptosis of lung adenocarcinoma induced by icotinib.

Methods: EGFR mutation was detected in lung adenocarcinoma cell line PC-9 by ARMS assay; The inhibitory rates of cell proliferation of PC-9 cells which were exposed to different concentrations of icotinib (0~100 μMol/L) for different time (24~72 h) respectively were evaluated by MTT assay; Apoptosis of PC-9 cells exposed to different concentrations of icotinib (0, 0.1, 1 and 10 μMol/L) for 48 h were evaluated by TUNEL assay; JAK2, STAT3, Bcl-2, Bax mRNA expressions were evaluated by Real-time PCR assay; The protein levels of P-STAT3 and IL-6 were evaluated by Western-blot assay.

The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.

The invasion and metastasis of malignant tumor cells lead to normal tissue destruction and are major prognostic factors for many malignant cancers. Long non-coding RNA (LncRNA) is associated with occurrence, development and prognoses of non-small cell lung cancer (NSCLC), but its mechanisms of action involved in tumor invasion and metastasis are not clear. In this study, we screened and detected the expression of LncRNA in two NSCLC lines 95D and 95C by using high throughput LncRNA chip.

Long-term survival for 93 months of limited-stage small cell lung cancer: A case report and literature review.

A 49-year-old man was diagnosed with small cell lung cancer in May 2005. Chemotherapy was started with 60 mg/day cisplatin iv drip (from days one to three), 2 mg topotecan (TP) hydrochloride iv drip (from days one to four), and traditional Chinese medicine (TCM) AiDi injection for anti-tumor. After four cycles, he underwent conformal radiotherapy with 56Gy/28 fractions in October 2005.

Identification of adipophilin as a potential diagnostic tumor marker for lung adenocarcinoma.

In our previous study, the upregulation of adipophilin in lung adenocarcinoma were identified compared with normal lung tissues by quantitative proteomics. In this study, our aim was to verify the result from quantitative proteomics, further investigate the relationship between adipophilin expression and clinicopathologic factors of lung cancer patients. The expression levels of adipophilin were examined in 10 pairs of lung adenocarcinoma and normal lung tissues using western blotting and the expression and cellular distribution of adipophilin were determined by IHC in 62 formalin-fixed and paraffin embedded primary lung cancer specimens.

Comparative membrane proteomic analysis between lung adenocarcinoma and normal tissue by iTRAQ labeling mass spectrometry.

Lung adenocarcinoma, the most common type of lung cancer, has increased in recent years. Prognosis is still poor, and pathogenesis remains unclear. This study aimed to investigate the membrane protein profile differences between lung adenocarcinoma and normal tissue.

Differential mitochondrial proteome analysis of human lung adenocarcinoma and normal bronchial epithelium cell lines using quantitative mass spectrometry.

Background: Lung cancer is one of the higher incidences of malignant tumors around the world. At present, tumor markers CEA, CA19-9, and CA-125 in serum are used for the diagnosis of lung cancer, however, fewer studies have shown tumor markers for early diagnosis. Therefore, using quantitative mass spectrometry, differential mitochondrial proteome analysis was performed, comparing human lung adenocarcinoma and normal bronchial epithelium cells.

[Clinical significance of detection of cathepsin X and cystatin C in the sera of patients with lung cancer].

Background And Objective: Cathepsin X (Cat X) has been identified as a member of cathepsin family. Studies have shown that Cat X is involved in tumorigenesis and tumor development of various cancers. The aim of this study is to investigate the relationship between the clinicopathological prognosis and the levels of Cat X and cystatin C in the serum of patients with lung cancer.

Adult Henoch-Schönlein purpura associated with small cell lung cancer: A case report and review of the literature.

The present study reports the case of a 53-year-old male who had been suffering from coughing and the presence of a blood-streaked sputum for >1 month. Chest computed tomography (CT) and a bronchoscopic brush smear were performed. The patient was subsequently diagnosed with small cell lung cancer (limited stage).