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Objective: To analyze the real-world growth pattern of very premature infants (VPI) with small for gestational age (SGA) after birth by using the ΔZ value of weight at discharge and evaluate the occurrence and risk factors of extrauterine growth retardation (EUGR).Methods: The clinical data of VPI with SGA were prospectively collected from 28 hospitals in seven different regions of China from September 2019 to December 2020. They were divided into the EUGR group and the non-EUGR group according to the criterion of ΔZ value of weight at discharge < –1.28.Results: This study included 133 eligible VPI with SGA. Following the criterion for the weight at discharge as the 10th percentile of the Fenton curve, the incidence of EUGR was found to be 98.50% (131/133), and following the criterion of ΔZ value of weight at discharge < –1.28, the incidence of EUGR was 36.84% (49/133). The birth weight, the 5-minute Apgar score, and the proportion of male infants in the EUGR group were lower than those in the non-EUGR group (P < 0.05). The average invasive ventilation time, cumulative duration of the administration of antibiotics, blood transfusion time, blood transfusion ratio, and total days of hospitalization were significantly higher in the EUGR group than those in the non-EUGR group (P < 0.05). The time to start enteral feeding, the quantity of milk added with human milk fortifier (HMF), the time to reach full fortification, the cumulative fasting time, the time to reach full enteral feeding, the duration of parenteral nutrition (PN), days to reach the target total calorie intake and oral calorie intake (both 110 kcal/kg/d), and the age of recovering birth weight in the EUGR group were significantly higher than that in the non-EUGR group (P < 0.05). The average weight gain velocity (GV) was significantly lower in the EUGR group than that in the non-EUGR group (P < 0.001). The incidences of patent ductus arteriosus with hemodynamic changes (hsPDA), neonatal necrotizing enterocolitis (NEC) ³ stage 2, late-onset sepsis (LOS), and feeding intolerance (FI) in the EUGR group were significantly higher than that in the non-EUGR group (P < 0.05). Multivariate logistic regression analysis showed that birth weight, sex (male), and GV were the protective factors for EUGR, while a long time to achieve full-dose fortification, slow recovery of birth weight, and NEC ³ stage 2 were the independent risk factors. Conclusion: SGA in VPI can reflect the occurrence of EUGR more accurately by using the ΔZ value of weight at discharge than using the p-value of weight. Strengthening enteral nutrition support, achieving full breast milk fortification more earlier increasing GV, shortening the recovery time of birth weight, and avoiding NEC can effectively reduce the incidence of EUGR.

OBJECTIVE: To investigate the incidence of extrauterine growth retardation (EUGR) and its risk factors in very preterm infants (VPIs) during hospitalization in China. METHODS: A prospective multicenter study was performed on the medical data of 2 514 VPIs who were hospitalized in the department of neonatology in 28 hospitals from 7 areas of China between September 2019 and December 2020. According to the presence or absence of EUGR based on the evaluation of body weight at the corrected gestational age of 36 weeks or at discharge, the VPIs were classified to two groups: EUGR group (n=1 189) and non-EUGR (n=1 325). The clinical features were compared between the two groups, and the incidence of EUGR and risk factors for EUGR were examined. RESULTS: The incidence of EUGR was 47.30% (1 189/2 514) evaluated by weight. The multivariate logistic regression analysis showed that higher weight growth velocity after regaining birth weight and higher cumulative calorie intake during the first week of hospitalization were protective factors against EUGR (P

OBJECTIVE: To construct risk prediction models for bronchopulmonary dysplasia (BPD) in preterm infants on postnatal days 3, 7, and 14. METHODS: A retrospective analysis was performed on the medical data of 414 preterm infants, with a gestational age of

OBJECTIVE: To study the correlation of fractional anisotropy (FA) on magnetic resonance diffusion tensor imaging with Neonatal Behavioral Neurological Assessment (NBNA) score in preterm infants, and to study the role of FA in evaluating white matter development from the perspective of imaging. METHODS: A prospective study was performed for 98 preterm infants who were admitted to the Neonatal Intensive Care Unit of the Third Affiliated Hospital of Zhengzhou University within 24 hours after birth from October 2016 to January 2020. According to the results of NBNA, they were divided into an abnormal group with 51 infants (NBNA score

OBJECTIVE: To assess white matter development in preterm infants with bronchopulmonary dysplasia (BPD) using fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values of diffusion tensor imaging (DTI). METHODS: Ninety-six infants with a gestational age of ≤ 32 weeks and a birth weight of < 1 500 g who were admitted to the neonatal intensive care unit within 24 hours after birth from August 2016 to April 2019 and underwent head MRI and DTI before discharge were enrolled. According to the discharge diagnosis, they were divided into BPD group with 48 infants and non-BPD group with 48 infants. The two groups were compared in terms of FA and ADC values of the same regions of interest on DTI image. RESULTS: There were no significant differences in the incidence rates of periventricular/intraventricular hemorrhage, periventricular leukomalacia, and punctate white matter lesions between the two groups (P > 0.05). Compared with the non-BPD group, the BPD group had significantly lower FA values and significantly higher ADC values of the posterior limb of the internal capsule, the splenium of the corpus callosum, the occipital white matter, the cerebellum, and the cerebral peduncle (P < 0.05). Compared with the non-BPD group, the BPD group had a significantly higher frequency of apnea, a significantly higher proportion of infants with pneumonia or mechanical ventilation, and a significantly longer duration of assisted ventilation (P < 0.05). CONCLUSIONS: BPD may has potential adverse effects to white matter development in preterm infants, leading to delayed white matter development. Therefore, it is necessary to pay attention to the neurological function of these infants.

OBJECTIVE: To investigate the risk factors for poor prognosis of neonatal bacterial meningitis. METHODS: A retrospective analysis was performed for the clinical data of 152 children with neonatal bacterial meningitis. According to their prognosis, they were divided into a good prognosis group with 122 children and a poor prognosis group with 30 children. The two groups were compared in terms of general status, initial symptoms, and laboratory findings, and the risk factors for poor prognosis were analyzed. RESULTS: Compared with the good prognosis group, the poor prognosis group had a significantly higher proportion of children with a very low birth weight, a peripheral blood white blood cell count (WBC) of < 5×10(9)/L or > 20×10(9)/L, a C-reactive protein level of > 50 mg/L, a cerebrospinal fluid (CSF) WBC of > 500×10(6)/L, a CSF glucose level of < 1 mmol/L, or a CSF protein level of > 2 g/L, as well as significantly higher positive rates of blood culture and/or CSF culture, Gram-positive bacteria, and Streptococcus agalactiae (P < 0.05). The multivariate logistic regression analysis showed that a CSF glucose level of < 1 mmol/L and a CSF protein level of > 2 g/L were independent risk factors for poor prognosis of neonatal bacterial meningitis. CONCLUSIONS: A CSF glucose level of < 1 mmol/L and a CSF protein level of > 2 g/L are risk factors for poor prognosis of neonatal bacterial meningitis.

OBJECTIVE: To investigate the pathogen composition and clinical features of preterm infants with sepsis, and to provide a basis for early identification and treatment of sepsis in preterm infants. METHODS: A retrospective analysis was performed for the clinical data of 371 preterm infants with sepsis who had a positive blood culture between January 2014 and May 2018. According to the time of onset, the preterm infants were divided into an early-onset group (an age of onset of < 7 days) with 73 preterm infants and a late-onset group (an age of onset of ≥ 7 days) with 298 preterm infants. The two groups were compared in terms of pathogen composition and clinical features (initial symptoms, laboratory examination results at the time of onset, comorbidities, and prognosis). RESULTS: There was a higher proportion of infants with Klebsiella pneumoniae infection in the late-onset group (P < 0.05), while there was a higher proportion of infants with Escherichia coli, Streptococcus agalactiae or Listeria infection in the early-onset group (P < 0.05). The early-onset group had a significantly higher proportion of infants with dyspnea than the late-onset group (P < 0.05). Compared with the late-onset group, the early-onset group had significantly shorter time to negative conversion of blood culture, duration of antibiotic use before infection, and indwelling time of deep venous catheterization (P < 0.05), and the late-onset group had a significantly higher incidence rate of neonatal necrotizing enterocolitis than the early-onset group (P < 0.05). The early-onset group had a significantly higher rate of treatment withdrawal than the late-onset group (P < 0.05). CONCLUSIONS: Preterm infants with sepsis lack typical clinical manifestations and laboratory examination results at the time of onset. There are certain differences in pathogen composition and clinical features between preterm infants with early-and late-onset sepsis. Possible pathogens for sepsis should be considered based on age in days at the time of onset and related clinical features.

OBJECTIVE: To study the clinical features and prognosis of preterm infants with varying degrees of bronchopulmonary dysplasia (BPD). METHODS: The clinical data of 144 preterm infants with a gestational age of < 32 weeks who were admitted to the neonatal intensive care unit from March 2014 to March 2016 and were diagnosed with BPD were collected. According to the severity of BPD, these preterm infants were divided into mild group with 81 infants and moderate/severe group with 63 infants. The two groups were compared in terms of perinatal risk factors, treatment, comorbidities, complications, and prognosis of the respiratory system. RESULTS: Compared with the mild BPD group, the moderate/severe BPD group had a significantly higher gestational age and rate of small-for-gestational-age (SGA) infants (P < 0.05), as well as a significantly higher rate of severe preeclampsia and a significantly lower rate of threatened preterm labor (P < 0.05). Compared with the mild BPD group, the moderate/severe BPD group had a significantly higher percentage of infants who needed mechanical ventilation at 2 weeks after birth, longer duration of mechanical ventilation, total time of oxygen therapy, and length of hospital stay, and higher incidence rates of pneumonia and cholestasis (P < 0.05), as well as a significantly lower application rate of caffeine citrate (P < 0.05). The multivariate logistic regression analysis showed that SGA birth (OR=5.974, P < 0.05), pneumonia (OR=2.590, P < 0.05), and mechanical ventilation required at 2 weeks after birth (OR=4.632, P < 0.05) were risk factors for increased severity of BPD. The pulmonary function test performed at the corrected gestational age of 40 weeks showed that compared with the mild BPD group, the moderate/severe BPD group had significantly lower ratio of time to peak tidal expiratory flow to total expiratory time, ratio of volume to peak tidal expiratory flow to total expiratory volume, and tidal expiratory flow at 25% remaining expiration (P < 0.05). The infants were followed up to the corrected gestational age of 1 year, and the moderate/severe BPD group had significantly higher incidence rates of recurrent hospital admission for pneumonia and recurrent wheezing (P < 0.05). CONCLUSIONS: SGA birth, pneumonia, and prolonged mechanical ventilation are associated with increased severity of BPD. Infants with moderate or severe BPD have poor pulmonary function and may experience recurrent infection and wheezing.

To study the effects of caffeine citrate on myelin basic protein (MBP) expression in the cerebral white matter of neonatal rats with hypoxic-ischemic brain damage (HIBD) and the related mechanism.Forty-eight seven-day-old Sprague-Dawley neonatal rats were randomly assigned to 3 groups: sham operation (n=16), HIBD (n=16) and HIBD+caffeine citrate (n=16). The rats in the HIBD and HIBD+caffeine citrate groups were subjected to left common carotid artery ligation, and then were exposed to 80 mL/L oxygen and 920 mL/L nitrogen for 2 hours to induce HIBD. The rats in the sham operation group were only subjected to a sham operation, without the left common carotid artery ligation or hypoxia exposure. Caffeine citrate (20 mg/kg) was injected intraperitoneally before hypoxia ischemia (HI) and immediately, 24 hours, 48 hours and 72 hours after HI. The other two groups were injected intraperitoneally with an equal volume of normal saline at the corresponding time points. On postnatal day 12, the expression of MBP in the left subcortical white matter was detected by immunohistochemistry, and the levels of adenosine A1 receptor mRNA and A2a receptor mRNA in the left brain were detected by real-time PCR.The expression of MBP in the left subcortical white matter in the HIBD group was lower than in the sham operation group (P0.05). The MBP expression in the HIBD+caffeine citrate group was significantly higher than in the HIBD group, but was still lower than the sham operation group (P0.05). Real-time PCR showed that the adenosine A1 receptor mRNA expression was significantly higher in the HIBD group than in the sham operation group, and it was significantly lower in the HIBD+caffeine citrate group than in the HIBD group (P0.05).Caffeine citrate can improve brain white matter damage following HIBD in neonatal rats and the protection mechanism might be related with the down-regulation of adenosine A1 receptor expression.

To investigate the effects of erythropoietin (EPO) on the neuronal proliferation and apoptosis in neonatal rats after infection-induced brain injury and the neuroprotective mechanism of EPO in neonatal rats with infection-induced brain injury.Twenty-six two-day-old neonatal rats were randomly divided into 3 groups: control group (intraperitoneally given an equal volume of normal saline), lipopolysaccharide (LPS) group (intraperitoneally given LPS 0.6 mg/kg), and EPO group (intraperitoneally given LPS 0.6 mg/kg and EPO 5 000 U/kg). These groups were injected with respective drugs for 5 consecutive days. Meanwhile, each group was intraperitoneally injected with 5-bromo-2'-deoxyuridine (BrdU) (50 mg/kg) once a day for 5 consecutive days. The expression of BrdU and cleaved Caspase-3 in the hippocampal dentate gyrus was detected by immunohistochemistry at 24 hours after the last injection.The number of neuronal cells in the hippocampal dentate gyrus in the LPS and EPO groups was significantly greater than in the control group (P0.05), but there was no significant difference between the LPS and EPO groups. The EPO group had a significantly higher number of BrdU-positive cells in the subgranular zone of hippocampal dentate gyrus than the LPS group (51±9 vs 29±6; P0.05), but a significantly lower number of BrdU-positive cells than the control group (51±9 vs 67±12; P0.05). The EPO group had a significantly lower number of cleaved Caspase-3-positive cells in the subgranular zone of hippocampal dentate gyrus than the LPS group (27.9±1.5 vs 34.0±1.3; P0.05), but a significantly higher number of cleaved Caspase-3-positive cells than the control group (27.9±1.5 vs 21.0±1.7; P0.05).EPO can promote hippocampal neuronal proliferation and reduce neuronal apoptosis in neonatal rats after infection-induced brain injury.

To study the clinical features of organic acidemia in neonates admitted to the intensive care unit.The clinical features of neonates from 15 neonatal intensive care units of Henan Province, who were diagnosed with congenital organic acidemia by gaschromatography-mass spectrometry (GC-MS) between June 2008 and August 2011 were retrospectively reviewed.Fifty neonates of 287 high risk neonates were confirmed as having or highly suspected to have inborn errors of metabolism. Of the 50 cases, 32 cases were diagnosed with organic acidemia disease, including 28 cases of methylmalonic acidemia, 2 cases of propionic acidemia, 1 case of maple syrup urine disease and 1 case of isovaleric acldemla. In most cases, disease onset occurred in the first week after birth in most of cases (75%). Neonates whose symptoms occurred immediately after or within a few hours of birth presented with serious conditions. Clinical manifestations were various and mainly related to neurologic, respiratory and gastrointestinal symptoms such as poor response, coma, drowsiness, abnormal muscle tone, convulsions, polypnea, dyspnea, milk refusal, diarrhea and jaundice. Initial symptoms were non-specific and included dyspnea, poor response, milk refusal, lethargy and seizures.Methylmalonic acidemia is a common inherited metabolic disease in the neonatal period. Clinical manifestations of organic acid metabolism abnormalities in neonates are atypical and early onset is associated with more serious conditions.

To understand the risk factors for respiratory distress syndrome (RDS) by comparing the perinatal conditions of preterm infants with different severities of RDS.A total of 667 preterm infants with RDS were classified into 4 groups according to the chest X-ray severity: grade I (217 cases), grade II (225 cases), grade III (126 cases) and grade IV (99 cases). The perinatal conditions of the preterm infants were reviewed retrospectively.There were no significant differences in the gender, the percentage of twins, the percentage of the younger one in twins, maternal age, the percentage of using antenatal corticosteroids, the percentage of premature rupture of membranes, the percentage of placental abruption, the delivery mode and the fertilization mode in preterm infants with different severities of RDS. With the increasing severity of RDS, the birth weight and the gestational age decreased, and the percentage of the infants with Apgar score ≤7 or maternal pregnancy-induced hypertension increased (P0.05).The severity of RDS is related to gestational age, birth weight and perinatal asphyxia in preterm infants.

Otoacoustic emissions (OAE) and auditory brainstem responses (ABR) are tests widely used in neonatal hearing screening. This study aimed to investigate the differences and clinical value of distortion product otoacoustic emissions (DPOAE) and ABR in hearing screening of high-risk neonates admitted to a neonatal intensive care unit (NICU).DPOAE and ABR were measured with the Smart-OAE analyser and the Smart-EP brain-stem electric response audiometry apparatus, respectively, in 600 high-risk neonates (1,200 ears). The testing results of DPOAE and ABR were compared.Of the 600 neonates (1,200 ears), the incidence of ABR abnormality (78.6%, 943/1,200) was remarkably higher than that of DPOAE abnormality (22.3%, 268/1,200). Two hundred and forty-one ears (20.8%) were negative and 252 (21%) were positive in both DPOAE and ABR tests. A total of 707 ears (58.9%) presented with a discordant result in DPOAE and ABR. The false positive and false negative rates of the DPOAE test were 6.0% (16/268) and 74.1% (691/932) respectively.In high-risk neonates the diagnostic value of DPOAE for identification of hearing loss, when used alone, is limited. The ABR test appears to be more reliable for hearing screening in high-risk neonates. It is suggested that hearing screening for high-risk neonates should be conducted with ABR first, followed by OAE after failure on ABR.

Objective To study the developmental changes of glutamic acid decarboxylase-67 (GAD-67, a GABA synthetic enzyme) in normal and hypoxic ischemic (HI) brain. Methods C57/BL6 mice on postnatal day (P) 5, 9, 21and 60, corresponding developmentally to premature, term, juvenile and adult human brain were investigated by using both Western blot and immunohistochemistry methods either in normal condition or after hypoxic ischemic insult. Results The immunoreactivity of GAD-67 was up regulated with brain development and significant difference was seen between mature (P21, P60) and immature (P5, P9) brain. GAD-67 immunoreactivity decreased in the ipsilateral hemisphere in all the ages after hypoxia ischemia (HI) insult, but, significant decrease was only seen in the immature brain. Double labeling of GAD-67 and cell death marker, TUNEL, in the cortex at 8h post-HI in the P9 mice showed that (15.6 +/- 7.0)%TUNEL positive cells were GAD-67 positive which was higher than that of P60 mice. Conclusion These data suggest that GABAergic neurons in immature brain were more vulnerable to HI insult than that of mature brain.

The study was to investigate the effect of different temperatures during hypoxia on brain injury in mice of different ages.Newborn C57/BL6 mice at 7 days or 21 days of life were subjected to left carotid artery ligation followed by exposure with 10% oxygen. The mice were kept in a incubator with a predetermined, constant temperature, either 34 degrees centigrade (Hypothermia group) or 36 degrees centigrade (Normothermia group). Brain injury was evaluated 7 days after hypoxia-ischemia (HI). Active caspase-3 and apoptosis-inducing factor (AIF) expressions in the brain tissue were detected by immunohistochemistry and Western Blot was used to evaluate the phosphor-Akt (P-Akt) expression in the brain tissue at 24 hrs post-HI.Brain injuries, including the cortex, hippocampus, striatum and thalamus injuries, occurred in the Normothermia group at 7 days post-HI. The brain cortex showed cystic cavitation in the postnatal day (P)7 pups mice and laminar infarct of the brain cortex was observed in P21 mice. In the Hypothermia group, the P7 mice did not present with laminar infarct of the cortex and had lower scores of neuropathological lesions in cortex, hippocampus, striatum and thalamus than P7 mice from the Normothermia group (P0.01); the cortex injuries were significantly relieved but the injuries of hippocampus, striatum and thalamus in P21 mice were similar to those from the Normothermia group. Active caspase-3 (7.0 +/- 5.6) and AIF positive cells (3.7 +/- 6.2) in the cortex of P7 mice from the Hypothermia group were significantly lower than those of the Normothermia group (51.5 +/- 23.2 and 31.8 +/- 22.4) at 24 hrs post-HI (P0.01). Wetstern Blot showed the P-Akt expression was obviously decreased in the ipsilateral hemisphere to the occlusion compared with that of the contralateral hemisphere after HI in the Normothermia group (P0.05), while in the Hypothermia group the P-Akt expression was not significantly different between the two hemispheres.Hypothermia has protective effects against HI insults. The protection was more pronounced for the immature brain than the mature brain.

p53-induced apoptosis is crucial in the development of hypoxic-ischemia (HI) brain damage and neurodegenerative disorders. Some experimental research has shown that a synthetic inhibitor of p53 can protect neurons against apoptosis. This study aimed to explore the expression of p53 in neonatal mice following HI brain damage and the effect of p53 inhibitor (pifithrin-alpha, PFT-alpha) on brain damage.HI was induced in 9-day-old mice pups by ligation of left carotid artery and 10% oxygen exposure for 55 minutes. The pups were sacrificed and the brains were taken out at 3, 8, 24, and 72 hrs post-HI. The brains were sectioned and stained with antibody against p53 and microtubule-associated protein 2 (MAP-2). PFT-alpha was injected intraperitoneally: in experiment 1, immediately after HI with different dosages (1, 2 and 8 mg/kg); in experiment 2, 2 mg/kg at different HI times (1 hr before HI, and immediately and 1 hr after HI). Control animals without HI received injections of 0.5% dimethyl sulfoxide. Brain damage was evaluated by gross morphology scoring at 72 hrs after HI.The number of p53 positive cells in the cortex, hippocampus and striatum of the ipsilateral hemisphere increased significantly and peaked at 3-8 hrs post-HI when compared with those of contralateral hemisphere as well as normal controls. The positive cells distributed mainly in the MAP-2 negative area. Both different dosages and different injection time PFT-alpha treatment did not reduce the extent of brain damage.The immunoactivity of p53 increased significantly as early as 3 hrs post-HI. The distribution area of p53 expression was consistent with that of brain damage. The p53 inhibitor PFT-alpha has no protective effects against HI brain damage in neonatal mice.

Recent studies suggest that hypothermia may be a potential treatment for perinatal hypoxic-ischemic (HI) brain damage. But the mechanisms of this effect are not well known. In the present study, the protective effect of systemic hypothermia as well as effect on apoptosis and associated biochemical events were investigated on neonatal rats with HI brain damage.Seven-day-old Wistar rats were subjected to left carotid artery ligation and hypoxia was persisted for 60 min. Immediately at the end of hypoxia, the animals were maintained either at 36 degrees C or 30 degrees C for 10 h at random. Caspase-2, 3 activity in brain homogenate was detected with Western blotting at 24 h post-HI (n = 8 for each group). Immunoactivity of microtubule-associated protein-2 (MAP-2), active caspase-3, apoptosis inducing factor (AIF) and oligonucleotide hairpin probe staining were detected at 72 h post-HI. The infarct volume, neuronal loss in CA(1) sector of hippocampus as well as brain injury scoring were calculated according to MAP-2 staining and hematoxylin and eosin staining.Caspase-2, 3 activities were much higher in the normothermia group [(27.7 +/- 14.7), (94.9 +/- 53.1) pmol/(min.mg protein)] at 24 h post-HI than those of hypothermia [(7.9 +/- 3.4), (21.1 +/- 18.7) pmol/(min.mg protein)] and normal control groups [(7.6 +/- 0.7), (12.9 +/- 0.5) pmol/(min x mg protein)] (P0.01). The activities were not significantly different between hypothermia group and normal control group. Western blotting showed that caspase-3 activation process was blocked by hypothermia. The number of active caspase-3 and AIF positive cells in the cortex of ipsilateral hemisphere was much higher in the normothermia group (median: 148.5; 22/field) than that of hypothermia group (median: 48.5; 9/field) (P0.05). The number of apoptotic cells as judged by oligonucleotide hairpin probe labeling was much higher in normothermia group (median: 144/field) than that of hypothermia group (median: 133/field) (P0.05). The brain injury scoring, infarct volume and neuronal loss in CA(1) area of hippocampus were much less in the hypothermia group [10.4 +/- 2.9; 40.5 +/- 34.8)mm(3); 25.7 +/- 11.5] than that of normothermia group [14.2 +/- 3.5; (73.9 +/- 22.4) mm(3); 37.4 +/- 10.6, P0.05].Systemic hypothermia for 10 h after hypoxia-ischemia seemed to be effective in reducing brain damage and the mechanism is associated with alteration of apoptotic pathway.