Objective To investigate the effect of hyperoxia on the transdifferentiation level of type Ⅱ alveolar epithelial cells (AEC Ⅱ) in vivo and in vitro,in order to illuminate the mechanism of epithelial injury in bronchopulmonary dysplasia (BPD).Methods Newborn Wistar rats were randomly devided into control group (room air inhalation) or model group (85％ oxygen inhalation) after birth.Lung tissue sampling and AEC Ⅱ isolation was conducted on 7 d,14 d,21 d.Type Ⅰ alveolar epithelial cells (AEC Ⅰ) marker aquaporin 5 (AQP5) and AEC Ⅱ marker surfactant protein C (SP-C) were examined by Western blot and florescent real-time PCR.AEC Ⅱ isolated from normal newborn rats was randomly devided into normoxia group (21％ oxygen) or hyperoxia group (85％ oxygen) after 24 h culture,and continued culturing for another 48 h in vitro.Then the morphological changes of cells were observed under inverted phase contrast microscope.The expression and location of markers for AEC Ⅰ and AEC Ⅱ was examined by immunofluorescence double staining.The protein expression of AQP5 and SP-C was evaluated by Western blot,and the mRNA expression of these markers was examined by florescent real-time PCR.Results In AEC Ⅱ isolated from the animal models,the AQP5 protein expression increased from 7 d while the SP-C expression decreased from 14 d in the model group comparing with the control group.In the model group,AQP5 mRNA expression increased and SP-C mRNA expression decreased since 7 d after hyperoxia exposure (P ＜ 0.05),with the difference between groups more obvious as exposure time extending.After culturing in vitro,AEC Ⅱ isolated from normal newborn rats expressed more AQP5 and less SP-C,with more cells double stained in the hyperoxia group compared with the normoxia group,examined by immunofluorescence double staining.The protein and mRNA examination results both showed that AQP5 expression increased and SP-C expression decreased in the hyperoxia group compared with the normoxia group (P ＜0.01).Conclusion After hyperoxia exposure,no matter in vivo or in vitro,the expression of AEC Ⅱ marker SP-C decreases while the expression of AEC Ⅰ marker AQP5 increases.These results indicate that the excessive transdifferentiation of AEC Ⅱ takes part in the recovery process after hyperoxia induced lung injury.

Objective To investigate the variation in expression and the significance of markers indi-cating typeⅠalveolar epithelial cells ( AECⅠ) and type Ⅱ alveolar epithelial cells ( AECⅡ) in hyperoxia induced bronchopulmonary dysplasia( BPD) model. Methods A total of 80 term normal Wistar rats were randomly devided into model group (85% oxygen) or control group (room air) within 12 h after birth,with 40 rats in each group. On day 7,day 14,day 21 after exposure,the pathological characteristics of lung tissues were observed using HE staining, the expression and location of AECⅠ marker aquaporin 5 ( AQP5 ) and AECⅡmarker surfactant protein-C ( SP-C) were examined using immunofluorescence double staining. West-ern blot analysis was employed to examine the expressions levels of AQP5 and SP-C proteins,while real-time PCR was used to evaluate the mRNA expression of AQP5 and SP-C. Results Alveolar developmental disor-der was observed in lung tissues of the model group,including fewer,larger,simplified alveoli,thicker alveo-lar walls,and fewer alveolar secondary septa. Immunofluorescence double staining showed increased and dis-organized AQP5 and SP-C expression, with significantly higher ratio of double-stained cells/SP-C positive cells in the model group ( P<0. 001 ) . Comparing to the control group, the expression of AQP5 and SP-C protein increased from 7 d after hyperoxia exposure,which continued to 21 d. The mRNA expression levels of these two markers both significantly increased in the model group compared with the control group, with AQP5 starting from 7 d while SP-C starting from 14 d after hyperoxia exposure (P<0. 05),and the differ-ence between two groups became more significant with the exposure time extending. Conclusion The expression of AECⅠ marker AQP5 and AECⅡ marker SP-C both increase in the lung tissues of hyperoxia induced BPD newborn rats,with more AECⅡ transdifferentiated into AECⅠ. These changes of the markers indicate that there is excessive transdifferentiation of AECⅡ in the recovery process after BPD lung injury.

Objective To investigate the ultrastructural alteration in brain tissues as well as the expression of bone morphogenetic protein(BMP) 4 and its effects on regulating myelination in the process of white matter injury development.Methods A total of 152 Sprague-Dawley newborn rats(3 days old) were randomly divided into white matter injury group(n=76) or control group(n=76).The white matter injury model was established by ligation of the right common carotid artery and hypoxic exposure(8% O2 and 92%N2),and samples were collected at 3d,7d,14d and 21d after operation.Morphological changes of the brain tissues were observed under a light microscope,while myelination was analyzed using a transmission electron microscope.The expression and location of BMP4 and myelin basic protein(MBP),a marker for myelination,was detected by immunohistochemistry staining,expression levels of BMP4 and MBP proteins were analyzed by Western blotting,and BMP4 mRNA expression was measured by real-time PCR.Results Observed under the light microscope,the cellular structure was clear,fibers arranged closely and orderly in the white matter of the control group.Whereas in the white matter injury group,sparse cells,loose mesh shaped white matter,and disorderly oriented fibers were observed.In the control group,myelin sheath had regular morphology,uniform density,and same thickness,observed using the transmission electron microscope.While in the white matter injury group,the myelin sheath was loosened,thinned,lamellar separated,and boundary obscured.Using immunohistochemistry staining,Western blot,and real-time PCR analyses,it was found that the protein and mRNA expression of BMP4 had no significant change with the increase of age in the control group,while it was rapidly increased with the extending of ischemic time in the white matter injury group.Comparing with the control group,the expression of BMP4 was significantly increased since 3d after operation in the white matter injury group(P<0.05),and the difference between two groups became more significant with the extending of ischemic time.The expression of MBP protein was analyzed by immunohistochemistry staining and Western blot,and a gradual increase was found in both groups with the increase of age.However,the expression of MBP protein was significantly decreased on 14d and 21d after operation in the white matter injury group compared with the control group(P<0.05).Conclusion Myelination disorders exists in white matter injury induced by ischemia-anoxemia.Meanwhile,the expression of BMP4 is significantly increased in the white matter injury group,indicating a possibility that BMP4 involves in the regulation of myelination disorders in white matter injury.

Mitochondrial disease refers to an energy metabolic disorder caused by dysfunction of oxidative phosphorylation system or pyruvate dehydrogenase complex as a result of mitochondrial DNA or nuclear DNA mutation.It can occur at any age arranging from newborn to adult, which is often presented as clinical syndromes.Common clinical manifestations in neonatal period include premature delivery, intrauterine growth restriction, hypotonia, dyspnea, convulsions, feeding difficulties, hyperlactic acid, etc, lacking of specificity.Neonatal onset syndromes include Leigh syndrome, mitochondrial encephalomyopathy-lactic acidosis and stroke-like episodes syndrome, Alpers syndrome, myocerebrohepatopathy spectrum disorder, Barth syndrome and Pearson syndrome.The diagnosis depends on the comprehensive analysis of clinical symptoms, biochemical tests, neuroimaging, histological tests and genetic tests.In most cases, there are few effective drugs.Gene therapy and exogenous mitochondrial transplantation are the directions of future exploration.

Neonatal cerebral infaraction(NCI)is the brain injury caused by cerebrovascular disease in neonates within 28 days, which can lead to poor outcome.At present, the etiology of NCI is still unclear, which may involve a variety of risk factors concerning maternal, placental and neonatal issues.The risk of developing NCI increases when risk factors increase.In order to indentify neonates with risk factors and diagnose NCI early, this review summarized the high-risk factors of NCI from three aspects, involving prenatal, intrapartum and postpartum stages.Timely intervention need to be given to improve the prognosis of neonates with NCI.

This article reported two cases of axillary artery thrombosis in extremely low/very low birth weight infants following the placement of a local arterial catheter, who hospitalized in Shengjing Hospital of China Medical Universityin in April 2023 and August 2022, respectively. Case 1: Before surgery for necrotizing enterocolitis, an arterial catheter was placed in the left axilla of the infant. On the same day, the infant developed cyanosis of the left upper limb and weakened radial artery pulse. Ultrasound examination confirmed the presence of left axillary artery thrombosis. Despite subcutaneous injection of low molecular weight heparin (LMWH) and plasma infusion, there was no improvement in blood circulation. The infant also exhibited reduced movement in the left upper limb and loss of radial artery pulse. Thrombolytic therapy with recombinant tissue-type plasminogen activator was administered. Six hours after the treatment, the radial artery pulse became palpable. Thrombolysis was then terminated, and anticoagulation with LMWH was supplied for two weeks. At one year and eight months of age, the infant had a weaker left-hand grip strength compared to the right, but the overall functionality was largely preserved. Case 2: The infant developed late-onset sepsis at 17 days old and had an arterial catheter placed in the axilla. Pale left upper limb was observed in the following day, and the brachial and radial artery pulses were absent. Vascular ultrasound indicated the presence of left axillary artery thrombosis. Anticoagulation therapy with subcutaneous injection of LMWH was provided, along with thrombolysis using urokinase. On the sixth day after thrombolysis, an ultrasound examination showed no thrombus-like echoes. At one year and eight months of age, the development and movement of the affected upper limb became normal.

This paper reports a case of neonatal lupus syndrome manifested by metabolic disease. A male neonate was admitted to the Children's Hospital of Soochow University due to poor response and vomiting for 1 day. Based on the clinical symptoms, including the patterned skin and a full anterior fontanelle, and a result of leukocytosis, neonatal sepsis was considered. Lysinuric protein intolerance was not excluded from the genetic metabolic disorders screening. The patient was positive for lupus-related autoantibodies and antinuclear antibodies, which were also found in his mother and elder sister. He had no functional variant of the SCL7A7 gene, a gene related to lysinuric protein intolerance, thereby the diagnosis of neonatal lupus syndrome manifested by metabolic disorders was confirmed. After treatment with methylprednisolone, the patient recovered well with no specific change in blood genetic metabolism at re-examination. Monthly follow-up after discharge found decreased antibody titers.