The innate immune system is critical to protect against microorganisms,but it is immature.Preterm newborn have to stay longer in NICU.They are vulnerable to infections.The common pathogen is coagulase-negative staphylococci which is the most cause of mortality for preterm newborn.So it is the key to understand the interaction between innate immune system of preterm newborn and pathogen.

Precocious puberty in children begins with the increased pulsatile secretion of the gonadotrophin-releasing hormone(GnRH)from hypothalamic.Recently,KISS1-GPR54 Was found to be a key factor to regulate the secretion of GnRH and the onset of puberty.Kisspeptin interacts with its receptor GPR54.which expressed on the hypothalamic GnRH neurons.and affects GnRH pulsatile release and the onset of puberty.GPR54 gene mutation causes the incidence of GnRH-dependent precocious puberty.

Coagulase-negative staphylococci,especially staphylococcus epidermidis (SE) is on the surface of skin and mucous membrane of human,and because of its high frequency,especially in hospital,it is thought to be an important opportunistic pathogen.SE is the common cause of preterm infection,and it has relationship with immature brain.Epidemiology supports the relationship among preterm,infection and brain injury.SE could lead to brain injury through Toll-like receptor mediated inflammation.

Melatonin has neuroprotective effect on hypoxic-ischemic brain damage(HIBD), which easily crosses the blood-brain barrier and plays neuroprotective role in reducing oxidative damage. Melatonin may be effective in preventing learing diabilities. It has been suggested that melatonin soporific effect is secondary to its ability to induce hypothermia. Neuroprotective effect of hypothmia has been proved. Howere, it is clear that hypothemia will not provide complete protection of HIBD and melatonin might augment protection of hypothemia in HIBD.

Procalcitonin (PCT)is a biomarker of early bacterial infection,and it can reflect severity of infection,and regarded as a prognostic factor.Community acquired pneumonia(CAP) is the main mortality and morbidity cause of children under 5 years old.The diagnosis of CAP mainly depends on clinical symptoms and chest radioactivity and regular blood test,and absent of specific indications,and mainly depends on clinicians experiences.The diagnosis and prognosis values in children CAP have been proved by many clinical trials.This paper reviews the clinical value of PCT on children CAP.

Objectives To investigate neuroprotective effect of melatonin on preterm rats brain damage after hypoxia-ischemia (HI). Methods In this study, 5-day-old Wistar rats were divided into four groups: normal saline group, melatonin group, HI+NS group and HI+melatonin group. HI was conducted by unilateral ligation of the left common carotid artery (ische-mia) and 50 min of hypoxia. Melatonin was injected at a dose of 5 mg/kg intraperitoneally three times:before ischemia, after hy-poxia and 24 h after the second dose. The pups were sacrificed at 24 h, 72 h, and 7 weeks after HI;for galectin-3 cells count at 72 h and 7 weeks;TNF-α, IL-1βprotein were measured in 24 h and 72 h after HI;and fear condition and elevated plus maze were tested in 7 weeks after HI. Results The number of galectin-3-positive cells was lower after melatonin treatment than vehi-cle treatment in 72 h and 7 weeks after HI (all P<0.05). TNF-αprotein and IL-1βprotein both increased at 24 h and 72 h after HI, and reduced after melatonin treatment (all P<0.05). Melatonin treatment improved memory ability and learning ability, re-duced anxiety in 7 weeks after HI. Conclusions Melatonin has long-term and short-term protective effect on developing brain damage after HI.

Objectives To study the influence of Staphylococcus epidermidis (SE) on the neonatal mice of different ages. Methods A total of 60 neonatal mice including postnatal day 1(PND1) and postnatal day 3(PND3) were divided into SE group, normal saline (NS) group and control group, with 20 mice each. Mice in SE group were intravenously injected with 50μl SE (108/ml). Mice in NS group were given 50μl NS and mice in control group was not intervened. On postnatal day 14, the brain, liver and spleen obtained from mice were weighted. Serial sections of paraffin-embedded brain tissue were used for the detec-tion of microtubule associated protein-2 (MAP-2) and myelin basic protein (MBP) by immumohistochemical staining, and then the areas and volumes of grey and white matter were calculated. Result The mortality of PND1 mice in SE and NS group was 60.0%and 40.0%, respectively, and there was no difference between two groups (P>0.05). The mortality of PND3 mice in SE and NS group was 10.0%and 0.0%, respectively, and there was no difference between two groups (P>0.05). There were no dif-ferences in body weight, body weight gain, spleen and liver weights and organ coefficient between PND1 and PND3 mice (P>0.05). In PND1 mice, the areas and volumes of grey and white matter were significantly smaller in SE group than those in NS group (P<0.05). However, in PND3 mice, there was no differences in areas and volumes of grey and white matter between SE and NS group (P>0.05). Conclusions SE infection can result in brain injury in PND1 mice, but has no effect on brain tissues of PND3 mice.

ObjectivesTo study the mechanism of brain damage caused byStaphylococcus epidermidis (SE) in mice. Methods A total of 80 neonatal mice of postnatal day 1 (PND1) were divided into SE group (48 mice), normal saline (NS) group (16 mice) and control group (16 mice). Mice in SE group were intravenously injected with 50 μl SE (108/ml). Mice in NS group were given 50 μl NS. Mice in control group were not intervened. At different time points after SE injection (6 h, 24 h, 72 h, 5 d, 7 d), the CFU of brain, blood, and spleen were calculated. Serial sections of parafifn-embedded brain tissue were used for detection of ionized calcium-binding adaptor moleculor1 (Iba-1) by immunohistochemical staining. The positive cells were calculated. ELISA was used to measure the levels of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-5 (IL-5), interleukin-6 (IL-6) of brain at 6 h and 24 h after SE injection.Results There was no SE in brain in different time points. The CFU was at the highest level at 6 h and then decreased after 24 h in blood and spleen. The Iba-1 positive cells in SE group were signiifcantly increased compared to NS group and control group at 24 h and 72 h (P<0.05). There was no difference of Iba-1 positive cells be-tween 24 h and 72 h after SE injection (P>0.05). The levels of TNF-α, IL-1β, IL-5, and IL-6 were signiifcantly higher in SE group than those in NS and control at 6 h and 24 h (P<0.05). The levels of TNF-α, IL-1β, IL-5, and IL-6 were signiifcantly lower in SE group at 24 h than those in SE group at 6 h (P<0.01).Conclusions It is suggested that cytokines produced by microglias may be the mediators of SE-caused brain damage.

Objective To investigate galectin3 on proliferation and migration of esophageal cancer Eca109 cells.Methods A lentiviral vector for over-expression of RNA targeting galectin3 was designed to transfect Eca109 cancer cells following plasmid-mediated transfection manual (Eca109/Gal3 cells).Inverted fluorescence microscope was used to observe the expression of EGFP.The proliferation of Eca109 cells was measured by cell counting Kit-8 assay.Eca109 cells apoptosis was determined by Annexin-V/7-AAD doublestaining.The migration capacity of Eca109 cells was determined in transwell assays.Western blot analysis was used to measure the expression of galectin3 protein.Results Galectin-3 expression was detected in Eca109 cells,with the Galectin3 expression in Eca109/Gal3 cells much more than non-transfected cells (t =14.33,P ＜ 0.05 ; t =10.28,P =0.037).Compared with non-transfected Eca109 cells,proliferation increased significantly in Eca109/Gal3 cells (t =-17.277,P ＜ 0.05 ; t =-13.4,P ＜ 0.05).Galectin3 evidently decreased in Eca109 cell apoptosis (t =3.053,P ＜ 0.05 ; t =5.446,P ＜ 0.05).Transwell migration assay showed that a greater number of Eca109/Gal3 cells crossed the artificial basement membrane compared with non-transfected Eca109 cells and negative control Eca109 cells (t =3.465,P ＜ 0.05; t =3.252,P ＜ 0.05).Conclusion Galectin3 expression is detected in transfected esophageal cancer Eca109 cells,whose overexpression can result in enhanced proliferation,migration,invasion as well as reduced apoptosis.These data indicate that in-depth research of galectin-3 may prove to be a potential molecular target for the treatment of esophageal cancer.

Nucleotide-binding oligomerization domain protein 2 (NOD2) involves in host immune responses to pathogens and regulates natural immunity and specific immunity by identifying the peptidoglycan of bacterial cell walls and cleavage product muramyl dipeptide.As a newly discovered intracellular pattern recognition receptor,NOD2 plays important roles in the development of primary hepatocellular carcinoma by gene mutate,inducing liver inflammatory reaction and activating relevant signaling pathways.