Are newborn rat-derived neural stem cells more sensitive to lead neurotoxicity?

Lead ion (Pb(2+) ) has been proven to be a neurotoxin due to its neurotoxicity on mammalian nervous system, especially for the developing brains of juveniles. However, many reported studies involved the negative effects of Pb(2+) on adult neural cells of humans or other mammals, only few of which have examined the effects of Pb(2+) on neural stem cells. The purpose of this study was to reveal the biological effects of Pb(2+) from lead acetate [Pb (CH 3 COO) 2 ] on viability, proliferation and differentiation of neural stem cells derived from the hippocampus of newborn rats aged 7 days and adult rats aged 90 days, respectively. This study was carried out in three parts. In the first part, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT viability assay) was used to detect the effects of Pb(2+) on the cell viability of passage 2 hippocampal neural stem cells after 48-hour exposure to 0-200 μM Pb(2+) . In the second part, 10 μM bromodeoxyuridine was added into the culture medium of passage 2 hippocampal neural stem cells after 48-hour exposure to 0- 200 μM Pb(2+) , followed by immunocytochemical staining with anti-bromodeoxyuridine to demonstrate the effects of Pb(2+) on cell proliferation. In the last part, passage 2 hippocampal neural stem cells were allowed to grow in the differentiation medium with 0-200 μM Pb(2+) . Immunocytochemical staining with anti-microtubule-associated protein 2 (a neuron marker), anti-glial fibrillary acidic protein (an astrocyte marker), and anti-RIP (an oligodendrocyte marker) was performed to detect the differentiation commitment of affected neural stem cells after 6 days. The data showed that Pb(2+) inhibited not only the viability and proliferation of rat hippocampal neural stem cells, but also their neuronal and oligodendrocyte differentiation in vitro. Moreover, increased activity of astrocyte differentiation of hippocampal neural stem cells from both newborn and adult rats was observed after exposure to high concentration of lead ion in vitro. These findings suggest that hippocampal neural stem cells of newborn rats were more sensitive than those from adult rats to Pb(2+) cytotoxicity.     

新生儿肺炎优势病原体及耐药情况分析

目的探讨新生儿肺炎优势病原体及耐药情况。方法对新生儿社区获得性肺炎和院内感染性肺炎的痰标本进行病原学检测及耐药情况。结果 1.社区获得性肺炎及院内感染性肺炎病原学特征都为细菌感染多于病毒感染;2.医院内感染性肺炎检测出的病原菌较单一;3.革兰氏阳性菌对青霉素耐药率较高,对氯唑西林钠较敏感,革兰氏阴性菌对头孢曲松钠敏感率高。结论新生儿院内感染性肺炎病原相对单一,耐药率低。     

Laparoscopic repair of bladder rupture in a neonate

Bladder rupture in a fetus is a rare occurrence. We report the first neonatal case of laparoscopic repair for prenatally diagnosed bladder rupture. A male neonate, who had presented with megacystis, bilateral hydronephrosis and hydroureters since 27 weeks‐of‐gestation, was delivered by emergency cesarean section because of sudden collapse of the bladder with massive ascites at 37 weeks‐of‐gestation. The diagnosis of bladder rupture was made by retrograde urethrocystography. Laparoscopic repair was carried out subsequent to urethral catheterization. Intraoperatively, laceration from the left side of the bladder dome to the posterior wall was observed. This tear was successfully repaired using a two‐layer interrupted suture without any postoperative complications. Laparoscopic repair could be the treatment of choice for bladder rupture, because it has the advantage of closure of the perforated site more certainly than bladder decompression alone, and with better cosmesis than open repair.     

新生儿社区和院内获得性肺炎的病原学特点及药敏分析

目的探讨新生儿社区获得性肺炎(CAP)和院内获得性肺炎(HAP)的病原分布和药敏情况。方法回顾性分析2010年1月—2014年12月因新生儿肺炎住院且痰培养阳性新生儿的临床资料。结果在3 564例CAP新生儿中共检出病原微生物4 383株,其中细菌3 584株、病毒771、真菌7株及非典型病原体21株。细菌以革兰阴性菌为主,3 045株(85.0%),细菌中排名前三的为肺炎克雷伯菌、大肠埃希菌及金黄色葡萄球菌;病毒以呼吸道合胞病毒为主,693株(89.9%)。在344例HAP新生儿中共检出病原微生物424株,其中细菌402株,真菌17株,呼吸道合胞病毒5株。细菌均为革兰阴性菌,未发现革兰阳性菌,排名前三的为肺炎克雷伯菌、大肠埃希菌及鲍曼不动杆菌。CAP与HAP新生儿中革兰阴性菌产ESBLs菌分别为26.9%、46.8%,差异有统计学意义(P?0.05)。CAP、HAP的肺炎克雷伯菌和大肠埃希菌均对阿米卡星、碳青霉烯类高度敏感。HAP的肺炎克雷伯菌对常用抗菌药物(除阿米卡星、喹诺酮类外)的敏感性普遍低于CAP,差异有统计学意义(P?0.05);HAP的大肠埃希菌对常用抗菌药物(除阿米卡星、喹诺酮类及碳青霉烯类外)的敏感性普遍低于CAP,差异有统计学意义(P?0.05)。此外,还发现耐碳青霉烯类的肠杆菌。结论新生儿肺炎病原菌以革兰阴性菌为主,其中CAP以肺炎克雷伯菌、大肠埃希菌及金黄色葡萄球菌为主,HAP以肺炎克雷伯菌、大肠埃希菌及鲍曼不动杆菌为主。HAP致病菌的产酶率和耐药性均普遍高于CAP,且有多重耐药趋势。     

NROB1基因错义突变致新生儿先天性肾上腺发育不良1例报告

目的探讨X连锁先天性肾上腺发育不良(AHC)的临床特点及诊断。方法回顾性分析1例AHC患儿的临床资料及基因检测结果,并复习相关文献。结果 2个月男性患儿,生后即出现体质量不增伴呕吐,伴有肾上腺功能不全失盐危象。基因检测发现NROB1基因错义突变,确诊为X-连锁先天性肾上腺发育不良。结论 X连锁先天性肾上腺发育不良是一种罕见病,诊断主要是通过临床表现、实验室检测及NROB1基因检测。     

Mitochondrial respiratory chain complex IV deficiency complicated with chronic intestinal pseudo‐obstruction in a neonate

A female infant born at 36 weeks gestational age with birthweight 2135 g, and who developed respiratory disorder, hyperlactacidemia and hypertrophic cardiomyopathy after birth, was admitted to hospital at 3 days of age. After admission, bilious emesis, abdominal distention, and passage disorder of the gastrointestinal tract were resistant to various drugs. Exploratory laparotomy was performed at 93 days of age, but no organic lesions were identified and normal Meissner/Auerbach nerve plexus was confirmed, which led to a clinical diagnosis of chronic intestinal pseudo‐obstruction (CIPO). She was diagnosed with mitochondrial respiratory chain complex IV deficiency on histopathology of the abdominal rectus muscle and enzyme activity measurement. This is the first report of a neonate with mitochondrial respiratory chain complex deficiency with intractable CIPO. CIPO can occur in neonates with mitochondrial respiratory chain disorder, necessitating differential diagnosis from Hirschsprung disease.     

High‐mobility group box‐1 release into fetal circulation from umbilical cord tissue and amniotic epithelium in fetal ischemia

We report the case of a baby with low birthweight born by emergency caesarean section at 33 weeks 2 days' gestation due to placental abruption. High‐mobility group box‐1 (HMGB‐1) and interleukin‐17 concentration in the umbilical cord blood were high at 55.7 ng/mL and 50.7 pg/mL, respectively. On immunostaining of umbilical cord and amniotic epithelium, HMGB‐1 was identified in the nuclei of vascular endothelial cells and cytoplasm of the surrounding cells in the umbilical cord. This suggests that, in the present case of placental abruption and subsequent ischemic placenta and fetus, the high level of HMGB‐1 observed was due to the release of HMGB‐1 into the umbilical cord blood from the vascular endothelial cells of the umbilical cord.