Objective To study the relationship between Caspase-12 expression and the hyperoxia-induced corpus callosum damage. Methods A total of 12 groups of C57 / BL6 mice were randomly assigned into hyperoxia group (80% O2 ) and control group (21% O2 ) at day 6 after birth (P6). The pups were sacrificed after 24 h and 48 h of hyperoxia exposure and at P10, P12, P15 and P30. Immunohistochemical ( IHC) method was used to detect the expression of myelin basic protein (MBP) in corpus callosum. Real-time PCR, Western Blot and IHC were used to detect the expression of mRNA and protein of Caspase-12 in corpus callosum. The corpus callosum apoptosis was measured using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling ( TUNEL ) method. Results The expression of MBP in hyperoxia group were significantly lower than the control group at P10 and P12 (P = 0. 004 and 0. 016); however, no significant differences existed between the two groups at P15 and P30 (P > 0. 05). The expression of Caspase-12 mRNA after 24 h and 48 h hyperoxia exposure were significantly higher than the control group [24 h: (1. 549 ± 0. 098) vs. (1. 080 ± 0. 101); 48 h:(1. 333 ± 0. 076) vs. (1. 022 ± 0. 089); P < 0. 05]. The expression of cleaved Caspase-12 protein after 24 h and 48 h hyperoxia exposure were also significantly higher than the control group [24 h: (1. 582 ± 0. 010) vs. (0. 994 ± 0. 078); 48 h: (1. 370 ± 0. 095) vs. (0. 978 ± 0. 069); P < 0. 05] . The Caspase-12 positive cell were significantly increased after 24 h and 48 h hyperoxia exposure comparing with the control group. The apoptosis index in hyperoxia group was significantly higher than the control group at P10 and P12 [P10: (18. 742 ± 2. 503) vs. (4. 587 ± 2. 353); P12 (36. 184 ± 3. 655) vs. (5. 351 ± 2. 678); P < 0. 05]. Conclusions Hyperoxia exposure induces corpus callosum damage in newborn mice. Over-expressed Caspase-12 may induce corpus callosum cell apoptosis excessively.

Objective To investigate the effect of catch-up growth on insulin resistance(IR) through analysis of biochemical and metabolic indices in premature infants.Methods There were 126 infants admitted in the Department of Neonatology,the Affiliated Hospital of Guiyang Medical College from December 2010 to December 2013 [factors which might affect the secretion of insulin(INS),C peptide and insulin-like growth factor-1 (IGF-1) were excluded].According to gestational age and birth weight,babies were divided into small for gestational age (SGA) group and appropriate for gestational age (AGA) group.And according to the age on follow-up,babies were divided into 1-to-6-month-old group,7-to-12-month-old group and ≥ 1-to-3 year-old group.All cases had 6 mL peripheral venous blood sampled in the early morning during fasting in the first week,and 6,12,24,36 months after birth.They were tested for levels of INS,C peptide,IGF-1,triglyceride (TC),total cholesterol (TG),high density lipoprotein cholesterol(HDL-C),low density lipoprotein cholesterol(LDL-C),fasting blood-glucose (FBG),albumin,prealbumin and creatinine respectively.At the same time,the physical parameters were measured,including weight,body length,and calculated insulin resistance index (IRI),Ponderal index,weight standard deviation score (SDS),and length SDS.Results (1) Catch-up growth after premature birth occupied 65.6％ (63/96 cases),whereas no catch-up growth occupied 34.4％ (33/96 cases) of study snbjects,and among them catch-up growth of 37 cases was better (8 cases of SGA,29 cases of AGA),26 cases showing catch-up growth(7 cases of SGA,19 cases of AGA),33 cases without catch-up growth(11 cases of SGA,22 cases of AGA).No statistical significance was found in the distribution of catch-up growth between SGA group and AGA group(P ＞ 0.05).(2) The LgIRI,LgINS of group with good catch-up growth was significantly lower than the group with no catch-up growth group (F =3.55,3.47) in infancy,but the level of IGF-1 and prealbumin was higher than that of no catch-up growth group (F =3.55,4.94),the difference had statistical significance (P ＜ 0.05) ; the better catch-up growth was associated with higher IGF-1 and prealbumin,but with lower LgIRI.(3) The risk factors for insulin resistance were SGA (OR =7.904,P =0.001),low birth weight ＜ 1 500 g (OR=8.737,P=0.019),and no catch-up growth (OR=11.706,P=0.000).Conclusions The better catch-up growth in infancy is associated with higher IGF-1 and prealbumin,but lower IR.The risk factors of IR include SGA,low birth weight and no catch-up growth,and the last being the major factor.

Objective:To evaluate the efficacy of neonatal resuscitation simulation exercise for perinatal medical personnel.Methods:From August 2020 to July 2021, perinatal medical personnel receiving simulated training of neonatal resuscitation in our hospital were prospectively enrolled. The professional backgrounds of the trainees were collected and their performances on both knowledge skills and behavioral skills were scored. The knowledge skills included pre-resuscitation preparation, initial resuscitation, positive pressure ventilation, tracheal intubation, chest compression and umbilical vein catheterization. The behavioral skills included situational awareness, problem solving, resource utilization, communication and leadership. SPSS 26.0 was used for data analysis.Results:Among the 200 participants, 127(63.5%) were neonatal/pediatric doctors and nurses, 65(32.5%) were obstetricians and midwives, 8(4.0%) were anesthesiologists and the ratio of doctors to nurses was 1.74∶1. The score of knowledge skills was (19.52±2.92) at the beginning of the simulation exercise and (27.02±2.72) at the end. The scores on preparation before resuscitation, initial resuscitation and positive pressure ventilation were significantly improved ( P<0.05). The score of behavioral skills was (16.60±2.34) at the beginning and (20.58±1.77) at the end. The scores of resource utilization, communication and leadership were significantly improved ( P<0.05). Conclusions:The simulation exercise provides multidisciplinary teamwork training for perinatal medical personnel, may significantly improve neonatal resuscitation skills and is worth promoting.

Objective:To investigate the clinical, genetic, and pathological features of nemaline myopathy type 8 (NEM8) caused by KLHL40 gene variation. Methods:The clinical data, gene sequencing results, and musculoskeletal pathophysiology of two cases (a pair of twins) with NEM8 admitted to our hospital in July 2022 were collected. CNKI, VIP, Wanfang, Yiigle, PubMed, Embase, and Web of Science Database were searched with the English and Chinese terms "nemaline myopathy type 8", "nemaline body myopathy type 8", and " KLHL40" from January 2007 to February 2023. The clinical, genetic, and musculoskeletal characteristics of the NEM8 cases were summarized using the descriptive statistical analysis method. Results:(1) Case report: The mother (G2P2) of the twins (Ⅳ-2 and Ⅳ-3) was conceived by IVF-embryo transfer and delivered at 37 +1 gestational weeks. The two cases were dizygotic twins whose maternal grandmother had lip and palate cleft. The first baby (Ⅳ-1) of the woman exhibited absent left pinna, contracture at the end of both fingers, talipes equinovarus in both feet and died of respiratory failure two hours after birth. Fetal edema and fetal movement delay in the twins and varus right foot in one twin were found during pregnancy. Both cases developed intrapartum asphyxia with the clinical manifestations of generalized muscle weakness, respiratory failure, dysphagia, multiple joint contractures, and fractures. The families withdrew the treatment and the twins died after maintaining life with ventilators for 53 days after birth. Whole exome sequencing of the pedigree found c.1779G>T (p.W593C) homozygous variants of the KLHL40 gene in the twins and c.1779G>T (p.W593C) heterozygous variants of the KLHL40 gene in the parents, both were de novo. Musculoskeletal pathophysiology indicated that muscle fibers are thin and round with a fetal shape and absent rod. (2) Literature review: Among the 29 cases of NEM8, including two current cases and 27 cases retrieved from 15 papers, eight cases terminated the pregnancies, and 21 were live births; seven cases (24.1%) with positive family history; 19 cases (65.5%) were found with abnormalities during pregnancy, including abnormal fetal movements, polyhydramnios, joint contracture, and fetal edema. Of the 21 live births, 20 cases had intrapartum asphyxia, 21 had postnatal respiratory failure, 20 had generalized muscle weakness, and 19 had dysphagia. Among the 29 cases, 17 cases (58.6%) were homozygous variants of the KLHL40 gene, and 12 cases (41.4%) were compound heterozygous variants. The detection rate of c.1516A>C(p.Thr506Pro) was the highest [72.4% (21/29)], followed by c.602G>A(p.Trp201*) [17.2% (5/29)]. Out of the 15 cases who underwent musculoskeletal pathological examination, all had abnormal muscle fiber size and morphology; 10 cases had rods. Conclusions:NEM8 should be considered for those with abnormal fetal movements, polyhydramnios, joint malformation, fetal edema during the fetal period and failure to establish respiration at birth as well as postnatal generalized muscle weakness, respiratory failure, dysphagia, multiple joint contractures, and fracture. Moreover, genetic detection should be performed as soon as possible. NEM8 can be diagnosed in ones with KLHL40 gene homozygous or compound heterozygous variants and musculoskeletal pathological results of abnormal size and shape of muscle fibers, regardless of the presence of rods.

Objective To investigate the effect of bone marrow mesenchymal stem cells(BMSCs)on the inflamma-tory response of lipopolysaccharide(LPS)induced acute lung injury(ALI)in mice.Methods 32 SPF KM mice,aged 4 weeks were randomly divided into four groups,control group,LPS group,dexamethasone treatment group(LPS+DEX)and BMSCs treatment group(LPS+BMSCs).The latter three groups were injected with LPS by tra-cheal puncture to establish mouse ALI model 24 h after modeling,BMSCs isolated from the femur of mice were in-jected into the caudal vein,and DEX were injected into caudal vein at the same time in LPS+DEX group for 3 consecutive days.On the 4th day after cell transplantation or 24 h after DEX injection,the survival quantity of mice was recorded,lung function was detected,and the wet/dry weight ratio(W/D)of lung was measured.Then in-flammatory cells in bronchoalveolar lavage fluid(BALF),lung pathological changes and serum inflammatory cyto-kines were collected.Green fluorescent protein(GFP)staining was used to observe the homing of BMSCs in lung tissues.The mRNA and protein expression of TLR4,MyD88 and NF-κB in lung tissues were detected by RT-PCR and Western blot assay respectively.Results Compared with the control group,LPS model group showed de-creased lung function,significantly increase in the W/D weight ratio of lung,inflammatory cytokines in serum and inflammatory cells in BALF,and severe damage in lung tissue.Compared with LPS group,LPS+DEX group and LPS+BMSCs group showed improved lung function,reduced lung tissue damage,significantly decrease in the W/D weight ratio of lung,inflammatory cytokines in serum and inflammatory cells in BALF.And the expression of TLR4-MyD88-NF-κB signaling pathway-related genes and proteins decreased,the survival quantity increased.Conclusion Homologous BMSCs transplantation can effectively treat LPS-induced acute lung injury,and the mechanism may be related to the regulation of TLR4-MyD88-NF-κB signaling pathway and the reduction of inflam-matory response.These findings provide the experimental basis for BMSCs homologous transplantation for ALI.