Infectious bone defect is bone defect with infection or as a result of treatment of bone infection. It requires surgical intervention, and the treatment processes are complex and long, which include bone infection control,bone defect repair and even complex soft tissue reconstructions in some cases. Failure to achieve the goals in any step may lead to the failure of the overall treatment. Therefore, infectious bone defect has been a worldwide challenge in the field of orthopedics. Conventionally, sequestrectomy, bone grafting, bone transport, and systemic/local antibiotic treatment are standard therapies. Radical debridement remains one of the cornerstones for the management of bone infection. However, the scale of debridement and the timing and method of bone defect reconstruction remain controversial. With the clinical application of induced membrane technique, effective infection control and rapid bone reconstruction have been achieved in the management of infectious bone defect. The induced membrane technique has attracted more interests and attention, but the lack of understanding the basic principles of infection control and technical details may hamper the clinical outcomes of induced membrane technique and complications can possibly occur. Therefore, the Chinese Orthopedic Association organized domestic orthopedic experts to formulate An evidence-based clinical guideline for the treatment of infectious bone defect with induced membrane technique ( version 2023) according to the evidence-based method and put forward recommendations on infectious bone defect from the aspects of precise diagnosis, preoperative evaluation, operation procedure, postoperative management and rehabilitation, so as to provide useful references for the treatment of infectious bone defect with induced membrane technique.

Objective:To analyze the role of perfusion index(PI)in assessing the severity of neonatal illnesses.Methods:A total of 502 newborns admitted to the Department of Neonatology within 24 hours of birth at Xinxiang Central Hospital from October 2018 to July 2019 were recruited.Neonatal critical illness score(NCIS)was graded within 24 hours of admission, and newborns were categorized into non-critical(NCIS>90 scores), critical(NCIS 70-90 scores)and extremely critical(NCIS<70 scores). PI was monitored in all newborns within 24 hours of birth in a resting state.A total of 502 PIs were recorded, including 341 cases of non-critical, 110 cases of critical and 51 cases of extremely critical.Results:The medium PI [ M( P25, P75)] of newborns in non-critical, critical and extremely critical groups were 1.80(1.40, 2.60), 0.96(0.74, 1.43)and 0.65(0.41, 1.10), respectively.PI values in extremely critical group was significantly lower than those in critical group and non-critical group( P<0.05). The medium PI [ M( P25, P75)] of full-term newborns, moderate/late preterm newborns and extremely/very preterm newborns were 1.70(1.20, 2.70), 1.60(1.10, 2.30) and 1.35(0.80, 2.30), respectively.PI in full-term newborns was significantly higher than those in moderate/late preterm newborns and extremely/very preterm newborns( P<0.05). PI was moderately positively correlated with NCIS in newborns( r=0.791, P<0.01). The area under the receiver operating characteristic curve of NCIS predicted by PI value was 0.846, and the prediction sensitivity and specificity were 85.0% and 70.8% when PI was 0.56. Conclusion:PI is correlated with NCIS in newborns, which is able to reflect the severity of neonatal illnesses.A low PI indicates severe conditions of neonatal illnesses.

Gestational diabetes mellitus (GDM) is the most common metabolic disorder during pregnancy, which seriously affects the normal development of the fetus.Blood glucose control during pregnancy is associated not only with recent adverse outcomes such as preterm birth, macrosomia, hypoglycemia, neonatal respiratory distress syndrome, electrolyte disorders, heart malformations and intestinal disorders, but also with long-term results such as conti-nued impaired glucose tolerance, obesity, metabolic syndrome, mental illness and eye disease.Correct understanding of adverse effects of GDM on newborn infants in the short and long term and their related mechanisms as well as timely prevention and treatment measures can significantly improve the outcome of pregnancy.This paper will make a summary of these problems.

Objective:To investigate the pathogenesis, precaution and treatment of neonatal congenital complete heart block (CCHB) in twins.Methods:The clinical data of a case of premature twins with neonatal CCHB from the Department of Neonatology, the First Affiliated Hospital of Xinxiang Medical University were retrospectively analyzed and related literature was reviewed.Results:(1)Case review: the 37-year-old gravida had no symptoms.Fetal ultrasound cardiogram(fUCG)at 23 weeks of gestation indicated bradycardia and CCHB.Then, the mother was diagnosed with undifferentiated connective tissue disease.After treatment with human immunoglobulin, dexamethasone and hydroxychloroquine, fUCG at 31 weeks of gestation still suggested CCHB.An emergency cesarean section was performed on the diagnosis of threatened preterm labor.With weakly positive neonatal antinuclear antibody (ANA), and positive Ro60 and Ro52 autoantibodies, twins were diagnosed with CCHB by 24 hour-Holter monitors.One of the twins was discharged with CCHB (ventricular rate of 80-90 times/min) after systemic therapy, but the weight increased to 2 200 g. The other one of the twins suffered from the sudden decrease of heart rate and blood pressure and finally died of sudden cardiac arrest.(2) Literature search: two cases in Chinese and 9 cases in English were reviewed.Among them, 9 cases were sjogren syndrome type A (SSA)/Ro and sjogren syndrome type B(SSB)/La related CCHB, and 2 cases were idiopathic CCHB.Conclusions:The placental transfer of anti-SSA or anti-SSB is an important mechanism of neonatal CCHB in twins, and other factors may also be involved.Current treatments are unsatisfactory.Most patients need pacemaker implantation.Early diagnosis and prenatal management can improve the prognosis.

Objective: To investigate the correlation between Toll like receptor 4 (TLR4) expression and apoptosis in periventricular leukomalacia (PVL) rat model induced by hypoxia-ischemia. Methods: One hundred and forty three-day-old sprague-dawley (SD) rats, which were divided into experimental group (ischemia-hypo-xia group) and control group (sham operation group) randomly, were used to establish a hypoxic model by ligating the right common carotid artery and inhaling gas mixtures with 60 mL/L oxygen and 940 mL/L nitrogen.The rats were killed 6 h, 12 h, 24 h, 3 d, 7 d after model reproducing and the brain tissues were used for the following experiments.The pathological changes and apoptosis of brain tissues were detected by way of hematoxylin and eosin (HE) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (Tunel) assay respectively, and TLR4 expression was detected by adopting immunohistochemistry and reverse-transcription polymerase chain reaction(RT-PCR). The data were analyzed by using the SPSS 19.0 software. Results: TLR4 expression in the modeling rat brain commenced to increase in 6 hours (0.541±0.069, 0.166±0.058)and reached the peak in 3 days(1.932±0.161, 0.300±0.039), and then began to decline in 7 days (1.242±0.109, 0.220±0.025) post hypoxia-ischemia.Compared with the control group, there were statistical significances at 6 h, 12 h, 24 h, 3 d and 7 d (all P<0.05). The apoptosis of brain ti-ssue cells in the modeling rat brain started to increase at 6 hours(21.33±3.50) and reached the peak in 3 days (35.97±4.20), and then began to decline in 7 days (31.02±4.22) post hypoxia-ischemia.Compared with the control group, there were statistical significance at 6 h, 12 h, 24 h, 3 d and 7 d (all P<0.05). The TLR4 expression was positively correlated with cell apoptosis (r=0.774, 0.575, all P<0.05). Conclusions In the rat model of PVL induced by hypoxia-ischemia, TLR4 is likely to injure the neural cell through apoptosis.

Objective: To investigate the effects of miR-23a-3p on proliferation, migration and apoptosis on human acute myeloid leukemia (AML) cells by targeting SMC1A. Methods: Microarray analysis was used to screen differentially expressed microRNAs and mRNAs in human AML cells. Real-time fluorescence quantitative PCR (RT-qRCR) was used to detect the expressions of miR-23a-3p and SMCA in human AML cell line U937. TargetScan database was used to analyze the correlation between miR-23a-3p and SMC1A. Double luciferase reporter gene was used to detect the interaction between miR-23a-3p and SMC1A. The effect of miR-23a-3p expression on the proliferation of U937 cells was detected by clonal assay. The migration, apoptosis, cell cycle and caspase-3 activity of U937 cells regulated by miR-23a-3p were detected by cell scratch assay and flow cytometry, respectively. Western blot was used to detect the expressions of Bax and Bcl-2 in U937 cells. Results: Compared with human normal monocyte SC group (1.00), the expression of miR-23a-3p in U937 cells was up-regulated (2.56±0.78) (P<0.01), while the expression of SMC1A was down-regulated (0.48±0.56, P<0.01). miR-23a-3p specifically bond to SMC1A 3′UTR and regulated the expression activity of SMC1A. Overexpression of miR-23a-3p promoted the proliferation and migration of U937 cells and inhibited the apoptosis of U937 cells, while up-regulation of SMC1A inhibited the proliferation and migration of U937 cells and promoted the apoptosis of U937 cells. The percentages of G₀/G1 phase, G₂/M phase and S phase cells in the negative control group were (37.48±0.21)%, (16.78±0.18)% and (45.74±0.15)% respectively, and those in the miR-23a-3p mimics group were (19.96±0.11)%, (41.69±0.24)% and (38.24±0.34)%, respectively. The difference was statistically significant (all P<0.05). The proportions of G₀/G₁ phase, G₂/M phase and S phase cells in the group of miR-23a-3p mimics+ pcDNA3.1-SMC1A were (36.88±0.21)%, (30.44±0.33)% and (32.88±0.16)%, respectively, without significant difference when compared with those of the miR-23a-3p mimics group (P>0.05). The relative expression levels of Bax and Bcl-2 protein in the negative control group were 0.55±0.45 and 0.31±0.54, respectively. Overexpression of miR-23a-3p inhibited the expression of Bax protein in U937 cells (0.23±0.13, P<0.001), promoted the expression of Bcl-2 protein (0.50±0.23, P<0.01), while SMC1A increased the expression of Bax protein in U937 cells (0.40±0.11, P<0.01), and inhibited the expression of Bcl-2 protein (0.37±0.15). In the negative control group, caspase-3 activity was (25.82±0.89)%. Overexpression of miR-23a-3p inhibited caspase-3 activity in U937 cells (3.64±0.56)%, P<0.01, while up-regulation of SMC1A promoted caspase-3 activity in U937 cells (15.29±0.85)%, P<0.01. Conclusion miR-23a-3p can inhibit the proliferation and migration and promote apoptosis of human AML cells by targeting SMC1A.

Objective To investigate the effects of miR?23a?3p on proliferation, migration and apoptosis on human acute myeloid leukemia ( AML) cells by targeting SMC1A. Methods Microarray analysis was used to screen differentially expressed microRNAs and mRNAs in human AML cells. Real?time fluorescence quantitative PCR (RT?qRCR) was used to detect the expressions of miR?23a?3p and SMCA in human AML cell line U937. TargetScan database was used to analyze the correlation between miR?23a?3p and SMC1A. Double luciferase reporter gene was used to detect the interaction between miR?23a?3p and SMC1A. The effect of miR?23a?3p expression on the proliferation of U937 cells was detected by clonal assay. The migration, apoptosis, cell cycle and caspase?3 activity of U937 cells regulated by miR?23a?3p were detected by cell scratch assay and flow cytometry, respectively. Western blot was used to detect the expressions of Bax and Bcl?2 in U937 cells. Results Compared with human normal monocyte SC group (1.00), the expression of miR?23a?3p in U937 cells was up?regulated (2.56±0.78) ( P＜0.01), while the expression of SMC1A was down?regulated (0.48±0.56, P＜0.01). miR?23a?3p specifically bond to SMC1A 3′UTR and regulated the expression activity of SMC1A. Overexpression of miR?23a?3p promoted the proliferation and migration of U937 cells and inhibited the apoptosis of U937 cells, while up?regulation of SMC1A inhibited the proliferation and migration of U937 cells and promoted the apoptosis of U937 cells. The percentages of G0／G1 phase, G2／M phase and S phase cells in the negative control group were ( 37.48 ± 0.21)%, (16.78±0.18)% and (45.74±0.15)% respectively, and those in the miR?23a?3p mimics group were (19.96±0.11)%, (41.69±0.24)% and (38.24±0.34)%, respectively. The difference was statistically significant (all P＜0.05). The proportions of G0／G1 phase, G2／M phase and S phase cells in the group of miR?23a?3p mimics+pcDNA3.1?SMC1A were (36.88± 0.21)%, ( 30.44± 0.33)% and ( 32.88± 0.16)%, respectively, without significant difference when compared with those of the miR?23a?3p mimics group ( P＞0.05). The relative expression levels of Bax and Bcl?2 protein in the negative control group were 0.55±0.45 and 0.31±0.54, respectively. Overexpression of miR?23a?3p inhibited the expression of Bax protein in U937 cells (0.23± 0.13, P＜0.001), promoted the expression of Bcl?2 protein ( 0.50 ± 0.23, P＜0.01), while SMC1A increased the expression of Bax protein in U937 cells (0.40± 0.11, P＜0.01), and inhibited the expression of Bcl?2 protein (0.37± 0.15). In the negative control group, caspase?3 activity was (25.82± 0.89)%.Overexpression of miR?23a?3p inhibited caspase?3 activity in U937 cells (3.64±0.56)%, P＜0.01, while up?regulation of SMC1A promoted caspase?3 activity in U937 cells ( 15.29 ± 0.85)%, P＜0.01. Conclusion miR?23a?3p can inhibit the proliferation and migration and promote apoptosis of human AML cells by targeting SMC1A.

Objective To investigate the effects of miR?23a?3p on proliferation, migration and apoptosis on human acute myeloid leukemia ( AML) cells by targeting SMC1A. Methods Microarray analysis was used to screen differentially expressed microRNAs and mRNAs in human AML cells. Real?time fluorescence quantitative PCR (RT?qRCR) was used to detect the expressions of miR?23a?3p and SMCA in human AML cell line U937. TargetScan database was used to analyze the correlation between miR?23a?3p and SMC1A. Double luciferase reporter gene was used to detect the interaction between miR?23a?3p and SMC1A. The effect of miR?23a?3p expression on the proliferation of U937 cells was detected by clonal assay. The migration, apoptosis, cell cycle and caspase?3 activity of U937 cells regulated by miR?23a?3p were detected by cell scratch assay and flow cytometry, respectively. Western blot was used to detect the expressions of Bax and Bcl?2 in U937 cells. Results Compared with human normal monocyte SC group (1.00), the expression of miR?23a?3p in U937 cells was up?regulated (2.56±0.78) ( P＜0.01), while the expression of SMC1A was down?regulated (0.48±0.56, P＜0.01). miR?23a?3p specifically bond to SMC1A 3′UTR and regulated the expression activity of SMC1A. Overexpression of miR?23a?3p promoted the proliferation and migration of U937 cells and inhibited the apoptosis of U937 cells, while up?regulation of SMC1A inhibited the proliferation and migration of U937 cells and promoted the apoptosis of U937 cells. The percentages of G0／G1 phase, G2／M phase and S phase cells in the negative control group were ( 37.48 ± 0.21)%, (16.78±0.18)% and (45.74±0.15)% respectively, and those in the miR?23a?3p mimics group were (19.96±0.11)%, (41.69±0.24)% and (38.24±0.34)%, respectively. The difference was statistically significant (all P＜0.05). The proportions of G0／G1 phase, G2／M phase and S phase cells in the group of miR?23a?3p mimics+pcDNA3.1?SMC1A were (36.88± 0.21)%, ( 30.44± 0.33)% and ( 32.88± 0.16)%, respectively, without significant difference when compared with those of the miR?23a?3p mimics group ( P＞0.05). The relative expression levels of Bax and Bcl?2 protein in the negative control group were 0.55±0.45 and 0.31±0.54, respectively. Overexpression of miR?23a?3p inhibited the expression of Bax protein in U937 cells (0.23± 0.13, P＜0.001), promoted the expression of Bcl?2 protein ( 0.50 ± 0.23, P＜0.01), while SMC1A increased the expression of Bax protein in U937 cells (0.40± 0.11, P＜0.01), and inhibited the expression of Bcl?2 protein (0.37± 0.15). In the negative control group, caspase?3 activity was (25.82± 0.89)%.Overexpression of miR?23a?3p inhibited caspase?3 activity in U937 cells (3.64±0.56)%, P＜0.01, while up?regulation of SMC1A promoted caspase?3 activity in U937 cells ( 15.29 ± 0.85)%, P＜0.01. Conclusion miR?23a?3p can inhibit the proliferation and migration and promote apoptosis of human AML cells by targeting SMC1A.

Objective: To investigate the feasibility of long noncoding RNA (lncRNA)_AK096792 as a clinical predictor of bronchopulmonary dysplasia (BPD) in preterm infants. Methods: All the cord blood(2-5 mL) of very low birth weight (VLBW) preterm infants born in Huai′an First Hospital Affiliated to Nanjing Medical University were collected from December 1, 2015 to December 1, 2017.Moreover, the peripheral blood(2 mL) of those VLBW infants diagnosed with BPD was also collected.A total of 36 infants with BPD were collected.Another 36 cases of premature children with VLBW were chosen as control group according to random number table.The relative content of lncRNA_AK096792 in cord blood and peripheral blood was detected by using real-time quantitative PCR (qPCR). Additionally, the correlation of lncRNA_AK096792 levels between cord and peripheral blood of BPD infants was analyzed.The sensitivity and specificity of lncRNA_AK096792 for BPD were analyzed by using receiver operating curve test. Results: (1)LncRNA_AK096792 was a common, evolutionarily conserved, non-coding RNA present in both mouse and human.(2) The expression level of lncRNA_AK096792 in peripheral blood was significantly higher than that in cord blood in BPD group[(463.3±352.0)% vs.(50.0±37.5)%], and the difference was significant(P<0.001), and they were highly correlated (r=0.825, P<0.001). (3) The level of lncRNA_AK096792 in cord blood in BPD group was signi-ficantly higher than that in non-BPD group [(484.3±280.5)% vs.(101.2±28.6)%], and the difference was significant(P<0.001). (4)When lncRNA_AK096792 served as a clinical predictor for BPD, the specificity was 83.3%, the sensitivity was 75.6%, and an area under the receiver operating characteristic curve was 0.88(P<0.001). Conclusions LncRNA_AK096792 is highly correlated with the development of BPD.The level of lncRNA_AK096792 in umbilical cord blood of premature infants can be used as an early predictive marker for BPD, it calls for further study.

Objective To investigate the effects of ω-3 polyunsaturated fatty acids(ω-3PUFAs)and ω-6 polyunsaturated fatty acids(ω-6PUFAs)on Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)signaling pathway,and the expressions of tumor necrosis factor-α(TNF-α),interleukin(IL)-1β and IL-6 in neonatal rats with brain injury induced by lipopolysaccharide (LPS). Methods Ninety-six neonatal rats were divided into control group,ω-3PUFAs group,ω-6PUFAs group,and LPS group by using random number table method. Intraperitoneal injection of LPS was performed in LPS group,ω-6PUFAs group and ω-3PUFAs group to establish models of rat brain injury. The rats in control group received 9 g/L saline. Twelve newborn rats were killed at 1 d or 5 d after intraperito-neal injection in each group for hippocampus selection. Real -time PCR and Western blot were used to detect the mRNA and protein expression levels of TLR4,NF-κB,TNF-α,IL-1β and IL-6. Results One day after mode-ling,TLR4,NF-κB,TNF-α,IL-1β and IL-6 mRNA expressions in ω-3PUFAs group (10. 63 ± 0. 07,5. 86 ± 1. 05,7. 65 ± 2. 29,5. 23 ± 1. 31,3. 36 ± 0. 72)were lower than those in ω-6PUFAs group (18. 83 ± 2. 10,8. 79 ± 2. 08,11. 95 ± 3. 23,10. 97 ± 2. 24,6. 37 ± 1. 17)and LPS group (15. 76 ± 1. 59,7. 13 ± 1. 10,9. 71 ± 2. 14,7. 83 ± 0. 85,4. 78 ± 0. 51),and the differences were all statistically significant(all P＜0. 05);which in ω-6PUFAs group were higher than those in LPS group,and the differences were all significant (all P＜0. 05). TLR4,NF-κB,TNF-α, IL-1β and IL-6 protein levels in ω-3PUFAs group (1. 57 ± 0. 11,1. 58 ± 0. 09,1. 55 ± 0. 09,1. 63 ± 0. 31,1. 36 ± 0. 12)were lower than those in ω-6PUFAs group (1. 96 ± 0. 17,2. 21 ± 0. 12,1. 95 ± 0. 23,1. 97 ± 0. 24,1. 77 ± 0. 17)and LPS group (1. 73 ± 0. 15,1. 87 ± 0. 10,1. 79 ± 0. 14,1. 83 ± 0. 15,1. 58 ± 0. 11)in 1 d,and the diffe-rences were all significant (all P＜0. 05),and those in ω-6PUFAs group were higher than those in LPS group (all P＜0. 05). Similarly,TLR,NF-κB,TNF-α,IL-1β and IL-6 mRNA and protein expression levels in ω-3PUFAs group (3. 78 ± 0. 88,3. 86 ± 0. 62,6. 26 ± 1. 94,3. 65 ± 1. 44,2. 11 ± 0. 87;1. 15 ± 0. 08,1. 32 ± 0. 10,1. 46 ± 0. 04, 1. 38 ± 0. 14,1. 21 ± 0. 09)were lower than those in ω-6PUFAs group (7. 76 ± 1. 65,5. 51 ± 0. 88,7. 96 ± 2. 13,5. 35 ± 1. 75,4. 88 ± 1. 35;1. 42 ± 0. 15,1. 51 ± 0. 36,1. 65 ± 0. 13,1. 72 ± 0. 23,1. 48 ± 0. 10)and LPS group (6. 21 ± 1. 87, 4. 98 ± 0. 73,7. 11 ± 2. 10,4. 84 ± 1. 75,4. 25 ± 0. 64;1. 35 ± 0. 13,1. 44 ± 0. 22,1. 59 ± 0. 10,1. 61 ± 0. 18,1. 35 ± 0. 07) in 5 d (all P＜0. 05),and which in ω-6PUFAs group were higher than those in LPS group,and the differences were sig-nificant (all P＜0. 05). Conclusion ω-6PUFAs can up-regulate the activity of TLR4,NF-κB,and reduce the re-lease of TNF-α,IL-1β and IL-6;and ω-3PUFAs can down-regulate the activity of TLR4,NF-κB,and reduce the release of TNF-α,IL-1β and IL-6,so it has a neural protective effect in brain injury induced by LPS.