OBJECTIVES: The neutrophil gelatinase-associated lipocalin (NGAL) level following non cardiac surgery is useful for predicting acute kidney damage. However, there is insufficient conclusive evidence as to whether NGAL can be used to predict subclinical AKI following non-cardiac surgery. METHODS: We measured serum NGAL and creatinine levels in 41 patients following non-cardiac surgery, and the increase of these variables was used to predict acute decreases in kidney function. RESULTS: The study included a total of 41 patients. The mean age was 64.65 ± 17.09 years. The serum creatinine concentration was increased 12 hours after surgery. The mean SD serum NGAL decreased after 4hours after surgery and continued to decrease after 12 hours after surgery. The incidence of subclinical AKI determined by the 4 hour serum NGAL level was 10(24.4%), and the incidence of serum creatinine elevation was 0(0.0%). The incidence of subclinical AKI determined by the 12 hour serum NGAL level was 4(9.8%), and the incidence of subclinical AKI determined by serum creatinine was 4(9.8%). The elevation of NGAL was more rapid than the serum creatinine 4 hours after surgery. CONCLUSIONS: We verified the usefulness of the serum NGAL level as a predictive factor for subclinical AKI after non-cardiac surgery.
Acute Kidney Injury* ; Creatinine ; Humans ; Incidence ; Kidney ; Lipocalins ; Neutrophils* ; Prognosis* ; Thoracic Surgery

Aberrant activation of Ras has been implicated in aggressiveness of breast cancer. Among Ras isoforms (H-, K-, and N-), H-Ras has been known to be primarily responsible for invasion and metastasis of breast cancer cells. Phosphorylation of serine (Ser) or threonine (Thr) is a key regulatory mechanism responsible for controlling activities and functions of various proteins involved in intracellular signal transduction. Peptidyl-prolyl Cis-trans isomerase NIMA-interacting 1, Pin1 changes the conformation of a subset of proteins phosphorylated on Ser/Thr that precedes proline (Pro). In this study we have found that Pin1 is highly overexpressed in human breast tumor tissues and H-Ras transformed human mammary epithelial (H-Ras MCF10A) and MDA-MB-231 breast cancer cells. Notably, Pin1 directly bound to the activated form of H-Ras harbouring a Ser/Thr-Pro motif. Pharmacologic inhibition of Pin1 reduced clonogenicity of MDA-MB-231 human breast cancer cells. Paclitaxel accelerates apoptosis in Pin1 silenced H-Ras MCF10A cells. MDR genes (MDR1 and MRP4) were significantly downregulated in MDA-MB-231 cells stably silenced for Pin1. We speculate that Pin1 interacts with GTP-H-Ras, thereby upregulating the expression of drug resistance genes, which confers survival advantage and aggressiveness of breast cancer cells under chemotherapy.