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| 1 | Intensive phototherapy vs.exchange transfusion for the treatment of neonatal hyperbilirubinemia:a multicenter retrospective cohort study显示文摘Background:Intensive phototherapy(IPT)and exchange transfusion(ET)are the main treatments for extreme hyperbilirubinemia.However,there is no reliable evidence on determining the thresholds for these treatments.This multicenter study compared the effectiveness and complications of IPT and ET in the treatment of extreme hyperbilirubinemia.Methods:This retrospective cohort study was conducted in seven centers from January 2015 to January 2018.Patients with extreme hyperbilirubinemia that met the criteria of ET were included.Patients were divided into three subgroups(low-,medium-,and high-risk)according to gestational week and risk factors.Propensity score matching(PSM)was performed to balance the data before treatment.Study outcomes included the development of bilirubin encephalopathy,duration of hospitalization,expenses,and complications.Mortality,auditory complications,seizures,enamel dysplasia,ocular motility disorders,athetosis,motor,and language development were evaluated during follow-up at age of 3 years.Results:A total of 1164 patients were included in this study.After PSM,296 patients in the IPT only group and 296 patients in the IPT plus ET group were further divided into the low-,medium-,and high-risk subgroups with 188,364,and 40 matched patients,respectively.No significant differences were found between the IPT only and IPT plus ET groups in terms of morbidity,complications,and sequelae.Hospitalization duration and expenses were lower in the low-and medium-risk subgroups in the IPT only group.Conclusions:In this study,our results suggest that IPT is a safe and effective treatment for extreme hyperbilirubinemia.The indication of ET for patients with hyperbilirubinemia could be stricter.However,it is necessary to have a contingency plan for emergency ET as soon as IPT is commenced especially for infants with risk factors.If IPT can be guaranteed and proved to be therapeutic,ET should be avoided as much as possible. | Meng Zhang Yang He Jun Tang Wenbin Dong Yong Zhang Benjin Zhang Hong Wan Quanmin Deng Lirong Guan Bin Xia Zhong Chen Min Ge Jing Zhao Wenxing Li Jingjun Pei Yi Qu Dezhi Mu | 2022 | Chinese Medical Journal2022，，5： | 7 |
| 2 | A new cell death program regulated by toll-like receptor 9 through p38 mitogen-activated protein kinase signaling pathway in a neonatal rat model with sepsis associated encephalopathy显示文摘Background:Sepsis,a serious condition with high mortality,usually causes sepsis associated encephalopathy(SAE)that involves neuronal cell death.However,the cell death programs involved and their underlying mechanisms are not clear.This study aimed to explore the regulatory mechanisms of different cell death programs in SAE.Methods:A neonatal rat model of SAE was established by cecal ligation and perforation.Survival rate and vital signs(mean arterial pressure and heart rate)were monitored,nerve reflexes were evaluated,and cortical pathological changes were observed by hematoxylin and eosin staining.The expression of pyroptosis,apoptosis,and necroptosis(PANoptosis)-related proteins,mitogen-activated protein kinase(MAPK),and its upstream regulator toll-like receptor 9(TLR9)were detected.The expression of TLR9 in neurons was observed by immunofluorescence staining.The ultrastructure of neurons was observed by transmission electron microscope.Results:First,PANoptosis was found in cortical nerve cells of the SAE rats.Meanwhile,the subunits of MAPKs,p38 MAPK,Jun N-terminal kinase,and extracellular signal-regulated kinase(ERK)were activated.After pharmacologically inhibiting each of the subunits,only p38 MAPK was found to be associated with PANoptosis.Furthermore,blocking the p38 MAPK signaling pathway activated necroptosis but inhibited apoptosis and pyroptosis.When necroptosis was pharmacologically inhibited,apoptosis and pyroptosis were reactivated.Finally,we found that the expression of TLR9,a regulator of MAPKs,was significantly increased in this model.After down-regulation of TLR9,p38 MAPK,and ERK signaling pathways were inhibited,which led to the inhibition of PANoptosis.Further analysis found that down-regulation of TLR9 improved the survival rate and reduced the pathological changes in SAE rats.Conclusions:Our study showed that the programs comprising PANoptosis are activated simultaneously in SAE rats.TLR9 activated PANoptosis through the p38 MAPK signaling pathway.TLR9 may work as a potential target for SAE treatment. | Ruixi Zhou Junjie Ying Xia Qiu Luting Yu Yan Yue Qian Liu Jing Shi Xihong Li Yi Qu Dezhi Mu | 2022 | Chinese Medical Journal2022，，12： | 3 |
| 3 | Influence of hypoxia-inducible factor 1-alpha on neuronal apoptosis in a rat model of hypoxia-or hypoxia-ischemia-induced brain injury显示文摘BACKGROUND: In addition to neuroprotective genes, the targeted genes of hypoxia-induciblefactor 1α (HIF-1α) include pro-apoptotic genes. However, the influence of HIF-1α on neuronalapoptosis in hypoxia-ischemia remains poorly understood.OBJECTIVE: To investigate the relationship between HIF-1α expression and neuronal apoptosis inhypoxia or hypoxia-ischemia brain injury and to determine the role of HIF-1α in regulating neuronalapoptosis.DESIGN, TIME AND SETTING: A randomized, controlled animal experiment was performed at theLaboratory of Children Neurology of Sichuan University between May 2006 and May 2007.MATERIALS: In situ cell death detected kit was provided by Roche, USA; rabbit anti-mouse HIF-1αpolyclonal antibody was purchased from Santa Cruz Biotechnologies, USA; rabbit anti-mousecleaved caspase-3 polyclonal antibody was purchased from Chemicon, USA.METHODS: A total of 36 Sprague Dawley rats aged 10 days were randomly assigned to 3 groups:sham-surgery, hypoxia, and hypoxia-ischemia, with 12 rats per group. The rats were treated at 3time points: 4, 8, and 24 hours, with 4 rats per time point. In the hypoxia-ischemia group, the rightcommon carotid artery was exposed and permanently ligated through a midline cervical incision. A2.5-hour exposure to hypoxia (8% O_2/92% N_2) was used to induce hypoxia-ischemia injury. In thehypoxia group, rats were exposed to hypoxia without ligation of the common carotid artery. In thesham-surgery group, the common carotid artery was exposed without ligation or hypoxia.MAIN OUTCOME MEASURES: Histopathological changes, HIF-1α and activated caspase-3 proteinexpression, integrated optical density of positive cells, and apoptosis-positive cells.RESULTS: Hematoxylin and eosin staining showed that neuronal degeneration and edema wasmost prominent at 24 hours after hypoxia-ischemia. HIF-1α protein expression was significantlyupregulated at 4 hours, peaked at 8 hours, and decreased at 24 hours after hypoxia orhypoxia-ischemia. HIF-1α protein expression was significant greater in the hypoxia andhypoxia-ischemia groups compared with the sham-surgery group (P < 0.01). Activated caspase-3protein expression began to increase at 4 and 8 hours following hypoxia or hypoxia-ischemia andwas significantly upregulated at 24 hours. Activated caspase-3 protein expression remained at lowlevels in the sham controls compared with the hypoxia and hypoxia-ischemia groups (P< 0.01).TUNEL staining showed that the number of apoptotic cells significantly increased at 24 hours afterhypoxia or hypoxia-ischemia. In addition, HIF-1α protein expression was greater in the hypoxiagroup compared with the hypoxia-ischemia group at the same time point (P< 0.05). However,activated caspase-3 expression and the number of TUNEL-positive cells were less in the hypoxiagroup compared with the hypoxia-ischemia group at the same time point (P < 0.05).CONCLUSION: HIF-1α played a neuroprotective role following hypoxia-ischemia brain injury. | Lihua Li Yi Qu Li Zhang Xihong Li Jinhui Li Meng Mao Xiudong Jin Dezhi Mu | 2009 | Neural Regeneration Research2009，4，12： | 2 |
| 4 | A Chinese Tuberous Sclerosis Complex Family and a Novel Tuberous Sclerosis Complex-2 Mutation显示文摘Tuberous sclerosis complex (TSC) is a relatively common autosomal dominant genetic disorder affecting l/14,000-1/6000 Western populations.The incidence of TSC in Chinese population is still unknown although case reports of Chinese TSC patients were documented.[1] The main clinical features of TSC include seizures,mental retardation,and the development ofhamartomas in multiple organs such as the skin,brain,lung,heart,and kidney.Indeed,the disease virtually manifests in every organ.[2] Two causative genes for TSC,TSC 1 gene on chromosome 9q34 and TSC2 gene on chromosome16p13,have been identified in 1997 and 1993 respectively.Approximately,70% of cases of TSC are de novo mutations.[3] Chinese TSC patients are more likely to have TSC2 missense and frame shift mutations.Here,we record one Chinese TSC family and it is novel frame shift mutation of TSC2. | Rong Luo Qianyun Cai Dezhi Mu | 2015 | Chinese Medical Journal2015，，1： | 2 |
| 5 | Expression of tumor necrosis factor α and neuronal apoptosis in the developing rat brain after neonatal stroke显示文摘 | Meng Mao Yimin Hua Xiangning Jiang Lihua Li Li Zhang Dezhi Mu | 2006 | Neuroscience Letters2006，，3： | 1 |
| 6 | Neuroprotection of brain-derived neurotrophic factor against hypoxic injury in vitro requires activation of extracellular signal-regulated kinase and phosphatidylinositol 3-kinase显示文摘 | Xiaomei Sun Hui Zhou Xiaoli Luo Shengfu Li Dan Yu Jiping Hua Dezhi Mu Meng Mao | 2007 | International Journal of Developmental Neuroscience2007，，3： | 1 |
| 7 | Erythropoietin for neonatal brain injury: opportunity and challenge显示文摘 | Tao Xiong Yi Qu Dezhi Mu Donna Ferriero | 2011 | International Journal of Developmental Neuroscience2011，，6： | 1 |
| 8 | Prevalence of neural tube defect pregnancies in China and the impact of gestational age of the births from 2006 to 2008: a hospital-based study显示文摘 | Jun Zhu Xiaohong Li Yanping Wang Dezhi Mu Li Dai Guangxuan Zhou Qi Li He Wang Juan Liang | 2012 | Journal of Maternal-Fetal and Neonatal Medicine2012，，9： | 1 |
| 9 | Hypoxia-inducible factor 1α and erythropoietin upregulation with deferoxamine salvage after neonatal stroke显示文摘 | Dezhi Mu Yun Sil Chang Zinaida S. Vexler Donna M. Ferriero | 2005 | Experimental Neurology2005，，2： | 1 |
| 10 | PirB restricts neuronal regeneration in developing rat brain followinghypoxia-ischemia显示文摘 | Hua Wang Ying Xiong Dezhi Mu | 2012 | Molecular Medicine Reports2012，，2： | 1 |
| 11 | Signaling pathway involved in hypoxia-inducible factor-1α regulation in hypoxic-ischemic cortical neurons in vitro显示文摘 | Li Zhang Yi Qu Chunlei Yang Jun Tang Xiaolan Zhang Meng Mao Dezhi Mu Donna Ferriero | 2009 | Neuroscience Letters2009，，1： | 1 |
| 12 | Erythropoietin for neonatal brain injury: opportunity and challenge显示文摘 | Tao Xiong Yi Qu Dezhi Mu Donna Ferriero | 2011 | International Journal of Developmental Neuroscience2011，，6： | 1 |
| 13 | Evaluation of oxidative stress in placenta of fetal cardiac dysfunction rat model and antioxidant defenses of maternal vitamin C supplementation with the impacts on P ‐glycoprotein显示文摘 | Yifei Li Jie Fang Kaiyu Zhou Chuan Wang Dezhi Mu Yimin Hua | 2014 | J Obstet Gynaecol Res2014，，6： | 1 |
| 14 | Pituitary deficiency due to primary pituitary apoplexy显示文摘To the editor:Primary pituitary apoplexy (PA) has few been reported in the cases of adolescents by any English publication.Unlike the secondary PA,primary PA often occurs in patients with pituitary tumor.It is rare and subclinical.Here we report an extremely rare case of chronic primary PA.The patient developed pituitary deficiency with symptoms like delay of puberty and low level of hormone.Therefore,we present the hormone characteristics,imaging findings and the briefly review other literature. | Qu Haibo Ning Gang Guo Yingkun Mu Dezhi | 2014 | Chinese Medical Journal2014，，11： | 0 |
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