Insulin Use Is Associated With Improved Outcomes in Critically Ill Patients With Acute Pancreatitis: A Retrospective Matched Cohort Study.

Background: Severe acute pancreatitis (SAP) has a mortality of 30% with no current targeted therapy. The potential protective effect of insulin on AP has been reported and needs to be confirmed. Thus, we aim to examine the effect of insulin treatment on the outcome of AP patients.

Association between serum-free thyroxine level and all-cause mortality in critically ill patients: a retrospective study from MIMIC-IV.

Background: Low thyroxine (T4) levels have been observed in critically ill patients; however, controversial results regarding T4 supplemental therapy are reported. The association between serum free T4 (FT4) levels and mortality in critically ill patients has not been fully established and needs to be clarified.

Methods: Data from the Medical Information Mart for Intensive Care (MIMIC)-IV were collected and analyzed.

Aaptamine derivatives with CDK2 inhibitory activities from the South China Sea sponge .

Three new aaptamines () together with two known derivatives () were isolated from the South China Sea sponge . The structures of all compounds were unambiguously elucidated by spectroscopic analyses as well as the comparison with literature data. All the compounds were evaluated for their cytotoxic activities against five human cancer cell lines including H1299, H520, SCG7901, CNE-2 and SW680 cells.

Scutellariabarbata D. Don extraction selectively targets stemness-prone NSCLC cells by attenuating SOX2/SMO/GLI1 network loop.

Ethnopharmacological Relevance: Scutellariabarbata D. Don extraction (SBE), a traditional Chinese medicine, has been proved effective against various malignant disorders in clinics with tolerable side-effects when administered alone or in combination with conventional chemotherapeutic regimens.

Aim Of This Study: Multi-drug resistance of cancer is attributed to existence of cancer stemness-prone cells that harbor aberrantly high activation of Sonic Hedgehog (SHH) cascade.

Dark Side of Cytotoxic Therapy: Chemoradiation-Induced Cell Death and Tumor Repopulation.

Accelerated tumor repopulation following chemoradiation is often observed in the clinic, but the underlying mechanisms remain unclear. In recent years, dying cells caused by chemoradiation have attracted much attention, and they may manifest diverse forms of cell death and release complex factors and thus orchestrate tumor repopulation cascades. Dying cells potentiate the survival of residual living tumor cells, remodel the tumor microenvironment, boost cell proliferation, and accelerate cancer cell metastasis.

Dying tumor cell-derived exosomal miR-194-5p potentiates survival and repopulation of tumor repopulating cells upon radiotherapy in pancreatic cancer.

Background: Tumor repopulation is a major cause of radiotherapy failure. Previous investigations highlighted that dying tumor cells played vital roles in tumor repopulation through promoting proliferation of the residual tumor repopulating cells (TRCs). However, TRCs also suffer DNA damage after radiotherapy, and might undergo mitotic catastrophe under the stimulation of proliferative factors released by dying cells.

MicroRNA-7 inhibits cell proliferation of chronic myeloid leukemia and sensitizes it to imatinib in vitro.

MicroRNA is a large class of non-coding small RNA that exerts critical roles in many physiological processes including cell proliferation. MicroRNA-7 (miR-7) has been considered as a tumor suppressor in most malignant tumors versus a tumor promoter in some other ones. However, its role in chronic myeloid leukemia remains unknown.

Inflammation-Related Pancreatic Carcinogenesis: Mechanisms and Clinical Potentials in Advances.

Chronic inflammation has long been considered critical in pancreatic carcinogenesis, and recently studies showed that some anti-inflammatory agents such as aspirin could potentially be used to attenuate pancreatic carcinogenesis. Several inflammation-related critical transcription factors and pathways such as NF-κB (nuclear factor κ-light-chain enhancer of activated B cells) and reactive oxygen species have been confirmed to be involved in carcinogenesis. However, its underlying mechanisms are far from clear, which largely limits further development of potential anticarcinogenesis drugs.

microRNA-7 impairs autophagy-derived pools of glucose to suppress pancreatic cancer progression.

Pancreatic cancer commonly addicts to aerobic glycolysis, and abnormally activates autophagy to adapt the stringent metabolic microenvironment. microRNA-7 (miR-7) was supposed to modulate various gastrointestinal cancer progression. We wonder whether miR-7 could destroy the reprogrammed metabolic homeostasis in pancreatic cancer via modulating the level of autophagy, and further affect tumor proliferation and survival.

Aspirin in pancreatic cancer: chemopreventive effects and therapeutic potentials.

Pancreatic cancer is one of the most aggressive malignancies with dismal prognosis. Recently, aspirin has been found to be an effective chemopreventive agent for many solid tumors. However, the function of aspirin use in pancreatic cancer largely remains unknown.

Cellular DDX3 regulates Japanese encephalitis virus replication by interacting with viral un-translated regions.

Japanese encephalitis virus is one of the most common causes for epidemic viral encephalitis in humans and animals. Herein we demonstrated that cellular helicase DDX3 is involved in JEV replication. DDX3 knockdown inhibits JEV replication.