Impact of COVID-19 pandemic on acute pancreatitis presentations, management, and in-hospital outcomes: a single-center, retrospective observational study from the northeast of China.

Background: Since initially detected in late December 2019, the novel coronavirus disease 2019 (COVID-19) outbreak rapidly swept the world, which has profoundly affected healthcare system and clinical practice in the management of gastrointestinal diseases.

Objectives: We aimed to evaluate the impact of COVID-19 pandemic on the pattern of hospital admissions and healthcare services for acute pancreatitis (AP).

Design: We conducted a retrospective observational cohort study using the anonymized electronic medical records.

Lnc-PFAR facilitates autophagy and exacerbates pancreatic fibrosis by reducing pre-miR-141 maturation in chronic pancreatitis.

Chronic pancreatitis (CP) is described as progressive inflammatory fibrosis of pancreas, accompanied with irreversible impaired endocrine and exocrine insufficiency. Pancreatic stellate cells (PSCs) are widely distributed in the stroma of the pancreas and PSCs activation has been shown as one of the leading causes for pancreatic fibrosis. Our previous study has revealed that autophagy is dramatically activated in CP tissues, which facilitates PSCs activation and pancreatic fibrosis.

Correction: Gut microbiota patterns associated with somatostatin in patients undergoing pancreaticoduodenectomy: a prospective study.

[This corrects the article DOI: 10.1038/s41420-020-00329-4.].

Gut microbiota patterns associated with somatostatin in patients undergoing pancreaticoduodenectomy: a prospective study.

Postoperative pancreatic fistula (POPF) is a common and dreaded complication after pancreaticoduodenectomy (PD). The gut microbiota has been considered as an crucial mediator of postoperative complications, however, the precise roles of gut microbiota in POPF are unclear. A prospective study was developed to explore the effects of somatostatin on gut microbiota and we aim to identify the microbial alterations in the process of POPF.

RB1CC1-enhanced autophagy facilitates PSCs activation and pancreatic fibrogenesis in chronic pancreatitis.

Chronic pancreatitis (CP) is described as a progressive fibro-inflammatory disorder of the exocrine disease, which eventually leads to damage of the gland. Excessive activation of pancreatic stellate cells (PSCs) is a critical participant in the initiation of CP. Autophagy is involved in multiple degeneration and inflammation in acute pancreatitis and CP.

Risk Factors for the Need of Surgical Necrosectomy After Percutaneous Catheter Drainage in the Management of Infection Secondary to Necrotizing Pancreatitis.

Objectives: This study aimed to assess the need of surgical necrosectomy after percutaneous catheter drainage (PCD) for infected necrotizing pancreatitis.

Methods: The clinical data of documented/suspected patients who were treated with a step-up approach were extracted and analyzed.

Results: Of the 329 patients enrolled, the initial PCD was performed at 12 (interquartile range, 9-15) days since onset and 35.

Early prediction of infected pancreatic necrosis secondary to necrotizing pancreatitis.

To assess the association between the clinical parameters within 48 hours of admission and the occurrence of infected pancreatic necrosis (IPN) during the late phase of necrotizing pancreatitis (NP).All patients were divided into 2 groups, the IPN and non-IPN groups. The clinical data were retrospectively analyzed.

Identification and characterization of a novel neuropeptide (neuropeptide Y-HS) from leech salivary gland of Haemadipsa sylvestris.

The present study was designed to identify immunomodulatory components from the leech salivary gland of Haemadipsa sylvestris. The Sephadex G-50, Resource(TM) S column chromatography and reverse-phase high performance liquid chromatography (RP-HPLC) were used to isolate and purify the salivary gland extracts (SGE). Structural analysis of isolated compounds was based on Edman degradation and matrix assisted laser desorption ionization time-of-flight mass spectrometer (MALDI-TOF-MS).

Long Noncoding RNA MALAT1 Promotes Aggressive Pancreatic Cancer Proliferation and Metastasis via the Stimulation of Autophagy.

Recently, pancreatic ductal adenocarcinoma (PDAC) has emerged as one of the most aggressive malignant tumors with the worst prognosis. Previous studies have demonstrated that long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is increased in pancreatic cancer and is identified as a diagnostic biomarker. Nonetheless, the molecular mechanism of elevated MALAT1 levels and tumor aggressiveness remains unknown.

A Novel Insulinotropic Peptide from the Skin Secretions of Amolops loloensis Frog.

Various kinds of biologically active peptides have previously been isolated from the skin secretions of Amolops loloensis frog, such as antimicrobial peptides, bradykinin-like peptides and algesic peptides. A novel insulinotropic peptide named amolopin was identified in A. loloensis frog's skin secretion.

[The clinical analysis of a step-up approach for severe acute pancreatitis: report of 121 cases].

Objective: To investigate the feasibility and clinical value of the step-up approach for severe acute pancreatitis (SAP).

Methods: Clinical data of 121 SAP patients admitted between January 2002 and December 2011 were retrospectively analyzed. Fifty-eight patients (37 males and 21 females, aged from 20 to 72 years, mean 47.

Nuclear factor-κB-dependent epithelial to mesenchymal transition induced by HIF-1α activation in pancreatic cancer cells under hypoxic conditions.

Background: Epithelial to mesenchymal transition (EMT) induced by hypoxia is one of the critical causes of treatment failure in different types of human cancers. NF-κB is closely involved in the progression of EMT. Compared with HIF-1α, the correlation between NF-κB and EMT during hypoxia has been less studied, and although the phenomenon was observed in the past, the molecular mechanisms involved remained unclear.

Dihydroartemisinin inhibits angiogenesis in pancreatic cancer by targeting the NF-κB pathway.

Purpose: Dihydroartemisinin (DHA) has recently shown antitumor activity in human pancreatic cancer cells. However, its effect on antiangiogenic activity in pancreatic cancer is unknown, and the mechanism is unclear. This study was aimed to investigate whether DHA would inhibit angiogenesis in human pancreatic cancer.

[Experimental study of the function and mechanism combining dihydroartemisinin and gemcitabine in treating pancreatic cancer].

Objective: To investigate the anti-tumor activity of combined gemcitabine with dihydroartemisinin, and the mechanism of the anti-tumor effect of gemcitabine enhanced by dihydroartemisinin on pancreatic cancer.

Methods: For cultured cells, cell growth was determined by the MTT assay and apoptosis was evaluated by flow cytometry analysis and confocal laser scanning microscope stained with Annexin V-FITC/PI. The nuclear extract for determining NF-kappaB DNA-binding activity was analyzed by EMSA, while nuclear P65 and its downstream gene expression was determined by Western blot assay.

Dihydroartemisinin inactivates NF-kappaB and potentiates the anti-tumor effect of gemcitabine on pancreatic cancer both in vitro and in vivo.

Gemcitabine is currently the best known chemotherapeutic option available for pancreatic cancer, but the tumor returns de novo with acquired resistance over time, which becomes a major issue for all gemcitabine-related chemotherapies. In this study, for the first time, we demonstrated that dihydroartemisinin (DHA) enhances gemcitabine-induced growth inhibition and apoptosis in both BxPC-3 and PANC-1 cell lines in vitro. The mechanism is at least partially due to DHA deactivates gemcitabine-induced NF-kappaB activation, so as to decrease tremendously the expression of its target gene products, such as c-myc, cyclin D1, Bcl-2, Bcl-xL.

[The effect of hyperbaric oxygen on acute pancreatitis through downregulating hypoxia-inducible factor.].

Objective: To observe the therapeutic effect of hyperbaric oxygen (HBO) on acute pancreatitis (AP) by downregulating hypoxia-inducible factor (HIF).

Methods: Forty Wistar rats were randomly divided into 4 groups (n = 10): sham group, AP group, normo-oxygen group (NP) and HBO group. At 4 hours after taurocholate-induced AP, the rats of NP group and HBO group were respectively treated with oxygen or HBO for 90 min.