Association Between High Serum Anion Gap and All-Cause Mortality in Non-Traumatic Subarachnoid Hemorrhage: A Retrospective Analysis of the MIMIC-IV Database.

Background: High serum anion gap (AG) on admission is often correlated with poor outcomes in critically ill patients; however, data in patients with non-traumatic subarachnoid hemorrhage (SAH) are lacking. Herein, we aimed to identify the association between serum AG and all-cause mortality in patients with non-traumatic SAH.

Methods: A retrospective analysis of data from the Medical Information Mart for Intensive Care (MIMIC-IV) database was performed on critically ill patients with non-traumatic SAH.

A hybridization chain reaction amplification strategy for fluorescence imaging of human telomerase activity in living cells.

A hybridized chain reaction (HCR)-based biosensing method has been developed for the imaging detection of intracellular telomerase activity. The telomerase-targeting responder-transmitter DNA complex (HPT) consisting of telomerase primer sequence (HP) and a HCR initiator (trigger) is transfected into cell plasma. In the presence of telomerase, HPT can be recognized and extended, producing plenty of triggers which initiate HCR amplification reaction.

[Metabolic Characteristics of Leucocyte-deplated and Suspended RBC Produced by Using Lipid Whole Blood During Routine Storage].

Objective: To investigate the differences of metabolic pathways of leucocyte-deplated RBCs prepared by using lipid whole blood and nomal blood during routine storage so as to provide some reference for clinical blood use.

Methods: Twenty U whole blood from 20 donors, including 10 U lipid blood and 10 U normal whole blood, were selected for preparing leukodepleted red blood cells, red blood cells were taken from storage bags on day 0, 14 and 35, respectively. Metabolites in the red blood cells were analyzed, red blood cell metabolic extracts were detected by UPLC-MS/MS.

Cisplatin-induced autophagy protects breast cancer cells from apoptosis by regulating yes-associated protein.

Breast cancer is a common cause of cancer‑related deaths in women. Treatment with cisplatin exhibits some therapeutic efficacy. However, treatment optimization is required, and the mechanisms underlying the cisplatin's proapoptotic effects remain unclear.

Leptin promotes the migration and invasion of breast cancer cells by upregulating ACAT2.

Background: Previously, it has been shown that obesity may be considered as a risk factor for breast cancer in postmenopausal women. Leptin, a hormone whose level is elevated in obesity, has been suggested to be involved in the development of breast cancer, and univariate survival analyses have shown that over-expression of ACAT2, an enzyme that is involved in the production of cholesteryl esters, may be associated with a poor prognosis. Here, we aimed to investigate the effect of leptin on the proliferation, migration and invasion of breast cancer cells, as well as to elucidate its underlying mode of action.

Pyruvate kinase M2 interacts with mammalian sterile 20-like kinase 1 and inhibits tamoxifen-induced apoptosis in human breast cancer cells.

Tamoxifen has been reported to be associated with antagonism of estrogen-mediated cell growth signaling and activation of estrogen receptor-independent apoptosis events. It has been demonstrated that mammalian sterile 20-like kinase 1 is a direct target of Caspases to amplify the apoptotic signaling pathway. Here, we presented that breast cancer MCF-7 and SKBR3 cells under treatment with 4-hydroxytamoxifen displayed decreased level of pyruvate kinase M2.

Invalidation of mitophagy by FBP1-mediated repression promotes apoptosis in breast cancer.

Fructose-1,6-bisphosphatase 1, a rate-limiting enzyme in gluconeogenesis, was recently shown to be a tumor suppressor. However, the functions of fructose-1,6-bisphosphatase 1 in the regulation of mitophagy and apoptosis remain unknown. Here, we investigated the effects of fructose-1,6-bisphosphatase 1 on mitophagy and apoptosis as well as their underlying mechanisms in breast cancer cells.

Leptin promotes breast cancer cell migration and invasion via IL-18 expression and secretion.

In recent years, crosstalk between tumor microenvironment and cancer cells have received increasing attention. Accumulating research data suggests that leptin, a key adipokine secreted from adipocytes, plays important roles in breast cancer development. In our study, the effects of leptin on polarization of tumor-associated macrophages (TAMs) and promotion of the invasiveness of tumor cells were investigated.

[BAY11-7082 inhibits proliferation and promotes apoptosis in breast carcinoma MCF-7 cells by inhibiting phosphorylation of ATP citrate lyase].

Objective: To investigate the effect of NF-κB inhibitor BAY11-7082 on proliferation and apoptosis of breast carcinoma MCF-7 cells and the underlying mechanism.

Methods: MCF-7 cells in the logarithmic growth phase were divided into control group, 5 μmol/L BAY11-7082 group and 10 μmol/L LY294002 group. After the treatment of BAY11-7082 and LY294002, the protein levels of ATP citrate lyase (ACL), phosphated-ACL (p-ACL), phosphated-Akt (p-Akt) and phosphated nuclear factor κB (p-NF-κB) were determined by Western blotting.