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OBJECTIVE To perform a retrospective analysis to determine the prevalence of hospital infection and associated risk factors and offer strategies in our neonatal intensive care unit(NICU).METHODS The study enrolled 1082 neonatal patients hospitalized between Jan 1,2006 to Dec 31,2007.RESULTS There were 58 nosocomial infections(NI) in 1082 neonatal patients,and the infection rate was 5.36%.The most common infection was superficial(62.07%).The mortality of NI was 6.90%.The lower gestational age and birth weight,were risk factors of NI.Logistic regression analysis indicated that mechanical ventilation and birth weight ≤1500g were independent risk ractors for NI(P
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Objective To investigate the effect and the possible mechanism of the apoptosis of neurons and the expression of bcl-2 gene in the neonatal rat brain after different courses of Dexamethasone (DXM). Methods Thirty-four Sprague-Dawley(SD) pregnant rats were randomized into four groups and received different courses of antenatal DXM at the dose of 0.8mg/(kg?d) intramuscularly: (1) Group 1 (n=8) received DXM on the 17th day of gestation only; (2) Group 2 (n=8) received DXM consecutively on the 17th,18th and 19th day of gestation; (3) Group 3 (n=10) received DXM consecutively for 4 days(on 17th,18th,19th and 20th day of gestation); (4) The control group (n=8) received equivalent volumes of isotonic saline intramuscularly consecutively for 4 days (gestational day 17, 18, 19, 20). On the postnatal day 1(P_1), day 7 (P_7) and day 14 (P_ 14 ), sixteen newborns in each group were randomly selected and sacrificed. The weights of the body and the whole brain were measured. Tunel was used to evaluate the apoptosis of neurons, and the content of bcl-2 protein was examined by improved Western Blot. Results (1) The brains weight of the newborn mice on P_1 were (0.301?0.030)g, (0.302?0.026)g, and (0.296?0.025)g in Group 1, 2 and 3, respectively and all significantly lower than that of the control [(0.363?0.041)g, P0.05). Conclusions Repeated doses of antenatal DXM therapy could significantly increase the apoptosis of neurons by down-regulate the bcl-2 expression and handicap the development of newborn mice′ brain.