Publications by authors named "Qingtian Zhu"

Background: Neutrophil extracellular traps (NETs) play a significant role in the development of acute pancreatitis (AP). The actin-binding protein LASP1 regulates proteins associated with the cytoskeleton, yet its precise involvement in NETs and AP remains to be elucidated.

Methods: To investigate the role of LASP1 in NETs and AP, several bioinformatics methods, such as weighted gene co-expression network analysis (WGCNA), differential analysis, and least absolute shrinkage and selection operator (LASSO) regression, were utilized to screen for feature genes based on the Gene Expression Omnibus (GEO) dataset.

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Background: Severe acute pancreatitis (SAP) is characterized by high mortality rates and various complications, including skeletal muscle atrophy, which significantly exacerbates its outcomes. Despite its clinical relevance, the mechanistic understanding of the relationship between skeletal muscle and the pancreas in SAP remains limited. Our study aimed to elucidate this "organ crosstalk" and its potential implications.

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The aging of pancreatic beta cells is closely associated with various diseases, such as impaired glucose tolerance, yet the underlying regulatory mechanisms remain unclear. In this study, we screened young and aged mouse pancreatic beta cells' high-throughput sequencing data from the GEO public database. Utilizing bioinformatics techniques, we identified the key regulatory factor YY1 in the aging process of pancreatic islets.

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  • * Transcriptome analysis showed that alterations in the glycolysis pathway and PGK1 correlate with inflammation and oxidative stress in acute pancreatitis, leading to increased PGK1 expression linked to PAC necrosis.
  • * Treatment with NG52, a PGK1 inhibitor, reduced pancreatic necrosis and inflammation, improved autophagy, and suggests that targeting PGK1 could provide new therapeutic strategies for acute pancreatitis.
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  • - Efferocytosis is an important process where macrophages clear dying cells, helping to control inflammation and prevent further cell death, but its role in acute pancreatitis (AP) is not well understood.
  • - The study found that injured pancreatic tissues from humans and mice showed increased levels of CD47, a molecule that signals cells not to be eaten, and identified its regulation by the transcription factor TRIM28 and the microRNA miR-133a.
  • - Using gene editing and other techniques, the research demonstrated that CD47's role in efferocytosis is key to preventing pancreatic cell death in AP, suggesting that targeting the TRIM28-miR133a-CD47 pathway might be a promising treatment strategy. *
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Introduction: To investigate whether increased intrapancreatic fat deposition (IPFD) heightens the risk of diseases of the exocrine and endocrine pancreas.

Methods: A prospective cohort study was conducted using data from the UK Biobank. IPFD was quantified using MRI and a deep learning-based framework called nnUNet.

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  • * In experiments, NAR treatment improved intestinal health by preserving crypts and villi, decreasing immune cell infiltration, and preventing cell apoptosis, as well as diminishing damage in human intestinal cells.
  • * The protective mechanism involves downregulation of the TRPV6 receptor, which helps lower calcium ion levels and reactive oxygen species, suggesting that NAR could serve as a therapeutic option for managing RIII.
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Bile acids are altered and associated with prognosis in patients with acute pancreatitis (AP). Here, we conduct targeted metabolomic analyses to detect bile acids changes in patients during the acute (n = 326) and the recovery (n = 133) phases of AP, as well as in healthy controls (n = 60). Chenodeoxycholic acid (CDCA) decreases in the acute phase, increases in the recovery phase, and is associated with pancreatic necrosis.

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Background And Purpose: Recent clinical studies have shown that serum high-density lipoprotein (HDL) levels are correlated with acute pancreatitis (AP) severity. We aimed to investigate the role of HDL in pancreatic necrosis in AP.

Experimental Approach: ApoA-I is the main constitution and function component of HDL.

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Ethnopharmacological Relevance: Acute pancreatitis (AP) is an acute inflammatory condition of pancreas with high morbidity and mortality, which has no effective medical treatment. Chaiqin chengqi decoction (CQCQD) has been clinically used for AP for many years in China. However, the underlying mechanisms are still unknown.

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Introduction: Irisin is a newly discovered myokine which links exercise to inflammation and inflammation-related diseases through macrophage regulation. However, the effect of irisin on the activity of inflammation related immune cells (such as neutrophils) has not been clearly described.

Objectives: The objective of our study was to explore the effect of irisin on the neutrophil extracellular traps (NETs) formation.

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Background: Acute pancreatitis (AP) is an inflammatory condition of the pancreas characterized by oxidative stress and inflammation in its pathophysiology. Acetyl-11-keto-β-boswellic acid (AKBA) is an active triterpenoid with antioxidant activity. This article seeks to assess the impact of AKBA on AP and investigate its underlying mechanisms.

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The inflammatory immune response mediated by neutrophils is closely related to the progression of acute pancreatitis. Previous studies confirmed that CD177 is a neutrophil-specific marker involved in the pathogenesis of conditions such as systemic vasculitis, asthma, and polycythemia vera. Neutrophil extracellular trap (NET) formation is a specific death program by which neutrophils release nuclear DNA covered with histones, granule proteins, etc.

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  • The study investigates the role of serum glycosylated hemoglobin A1c (HbA1c) levels in assessing the severity and outcomes of acute pancreatitis (AP), focusing on two groups: normal HbA1c levels (<6.5%) and high levels.
  • It was found that higher HbA1c levels correlate with increased disease severity, complications, and the risk of organ failure in AP patients, with the optimal cutoff for predicting organ failure at 7.05%.
  • The results suggest that better glycemic control may lead to improved outcomes in AP, emphasizing the importance of monitoring HbA1c levels prior to the onset of the condition.
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Acute pancreatitis (AP) is a local and/or systemic inflammatory disease that starts with acinar cell injury and necrosis; it has no effective medical treatment and thus remains a life-threatening condition. Interleukin-37 (IL-37), a natural immunomodulator, has demonstrated an antiinflammatory effect; however, the role of IL-37 in AP remains unknown. The serum IL-37 levels of 39 healthy controls and 94 patients with AP were measured.

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  • The study examines how elevated serum ferritin (SF) levels relate to the severity of acute pancreatitis (AP), noting SF is an indicator of oxidative stress and inflammation.
  • An analysis of 200 AP patients revealed that nearly half had high SF levels, which were linked to a higher severity of the condition and increased systemic inflammatory response.
  • The study concluded that SF levels can effectively predict the severity of AP and the likelihood of organ failure in affected patients.
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Recently, deep learning based multi-view stereo (MVS) networks have demonstrated their excellent performance on various benchmarks. In this paper, we present an effective and efficient recurrent neural network (RNN) for accurate and complete dense point cloud reconstruction. Instead of regularizing the cost volume via conventional 3D CNN or unidirectional RNN like previous attempts, we adopt a bidirectional hybrid Long Short-Term Memory (LSTM) based structure for cost volume regularization.

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Background: Innate immunity and metabolites link to the pathogenesis and severity of acute pancreatitis (AP). However, liver metabolism and its role in immune response and AP progression remain elusive. We investigated the function of liver metabolism in the pathogenesis of AP.

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The excessive inflammatory response mediated by macrophage is one of the key factors for the progress of acute pancreatitis (AP). Paeonol (Pae) was demonstrated to exert multiple anti-inflammatory effects. However, the role of Pae on AP is not clear.

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Background: The gastrointestinal microbiota is emerging as an important mediator in intestinal metabolism, such as vitamin D absorption.

Methods: To elucidate the causality of microbiota and vitamin D, we used linkage disequilibrium score (LDSC) regression and two-sample Mendelian randomization (MR) methods with largest genome-wide association study (GWAS) summary statistics to identify specific taxa that are linked to serum 25-hydroxyvitamin D (25(OH)D).

Results: We found that Ruminiclostridium9 was significantly genetically correlated with 25(OH)D at nominal significance (r = 0.

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As a calcium-regulated protein, CaMK II is closely related to cell death, and it participates in the development of pathological processes such as reperfusion injury, myocardial infarction, and oligodendrocyte death. The function of CaMK II activation in acute pancreatitis (AP) remains unclear. In our study, we confirmed that the expression of p-CaMK II was increased significantly and consistently in injured pancreatic tissues after caerulein-induced AP.

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Hypoxia-inducible factor-1α (Hif1α) is activated in hypoxia and is closely related to oxidative stress, immunity and cell metabolism. Recently, it is reported that Hif1α is involved in atherosclerosis, ischemia-reperfusion (I/R) injury, alcoholic liver disease and pancreatic tumors. In this study, we found that Hif1 signal pathway is significantly changed in pancreas of acute pancreatitis (AP) mice.

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Background And Purpose: Pyroptosis is a lytic form of pro-inflammatory cell death characterised as caspase 1 dependent with canonical NLRP3 inflammasome-induced gasdermin D (GSDMD) activation. We aimed to investigate the role of acinar pyroptotic cell death in pancreatic injury and systemic inflammation in AP.

Experimental Approach: Pancreatic acinar pyroptotic cell death pathway activation upon pancreatic toxin stimulation in vitro and in vivo was investigated.

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Method: Repeated caerulein injection was used to induce AP and chronic pancreatitis (CP) models in mice. The histopathological and serological changes were examined for evaluating the severity of the AP model, and flow cytometry was used for detecting macrophage phagocytosis and phenotype. Meanwhile, clodronate liposomes were used for macrophage depletion in mice.

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Acinar cell necrosis is one of the most prominent pathophysiological changes of acute pancreatitis (AP). Asiaticoside (AS) is a triterpene compound with confirmed apoptosis-and necrosis-related activities. However, the specific effects of AS on AP have not been determined.

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