Background: Acute renal failure is a common emergency and esspecial dangerous in the neonatal disease group, account for from 8% to 24% of among total patients to be treated at Intensive Care Unit with the high rate of mortality and complication. The mortality rate due to acute renal failure in neonatal group account for from 24.4% to 66,7%. Objectives: This study aims to learn about the clinical and laboratory characteristics as well as some risks factors of neonatal acute renal failure. Subjects and method:A descriptive, retrospective study was conduct on 64 patients without diagnosed of acute renal failure in control group and other 32 cases of acute renal failure whom treated at Neonatal Department of National Hospital for Pediatric from 1st January 2005 to 31st March 2006. Results:The diagnosis was often done in the 1st week of life and the incidence occurred in boy more than in girl.The average reatininernie\r\n', u'was 251.7\xb112.96 \xb5ol/l, the electrical disorder (in which hyperkaliernie: 78.1%, hyponatrernie: 46.9%), anernie was 18.7%, acidosis netabolique was 71.9%. Risk factors of neonatal acute renal failure: the pre-puerperal eclampsia (p = 0.023, OR=1.23), infection (p <0.001, OR = 9.53), suffocation (p <0.05, OR = 2.489), respiratory failure (p <0.001, OR = 2.489). Conclusion: The clinical signs were hyponurie and anuria, oederne and arterial hypertension.\r\n', u'\r\n', u'
Acute Kidney Injury/ diagnosis ; pathology ; Infant

Objective: To investigate the inhibited effect of epigallocatechin-3-gallate (EGCG) on the expression of NPM1 in IMS-M2 cells harboring the NPM1 mutations. Methods: Cell proliferation assay was performed to test the effects of EGCG on cell growth of IMS-M2 cells harboring the NPM1 mutations. Western blot analysis were performed to test the protein expression of NPM1, AKT, those associated with apoptosis. Results: EGCG can down-regulate the expression of NPM1 in IMS-M2 cells harboring the NPM1 mutations. Moreover, EGCG also suppressed the cell proliferation and induced apoptosis in IMS-M2 cells. Conclusions: The results suggested that EGCG could be considered as a reagent for treatment of AML patients with NPM1 mutations.

OBJECTIVETo investigate the inhibited effect of epigallocatechin-3-gallate (EGCG) on the expression of NPM1 in IMS-M2 cells harboring the NPM1 mutations.

METHODSCell proliferation assay was performed to test the effects of EGCG on cell growth of IMS-M2 cells harboring the NPM1 mutations. Western blot analysis were performed to test the protein expression of NPM1, AKT, those associated with apoptosis.

RESULTSEGCG can down-regulate the expression of NPM1 in IMS-M2 cells harboring the NPM1 mutations. Moreover, EGCG also suppressed the cell proliferation and induced apoptosis in IMS-M2 cells.

CONCLUSIONSThe results suggested that EGCG could be considered as a reagent for treatment of AML patients with NPM1 mutations.