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 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.

The differentiation and maturation of oligodendrocyte precursor cells (OPCs) is essential for myelination and remyelination in the CNS. The failure of OPCs to achieve terminal differentiation in demyelinating lesions often results in unsuccessful remyelination in a variety of human demyelinating diseases. However, the molecular mechanisms controlling OPC differentiation under pathological conditions remain largely unknown. Myt1L (myelin transcription factor 1-like), mainly expressed in neurons, has been associated with intellectual disability, schizophrenia, and depression. In the present study, we found that Myt1L was expressed in oligodendrocyte lineage cells during myelination and remyelination. The expression level of Myt1L in neuron/glia antigen 2-positive (NG2) OPCs was significantly higher than that in mature CC1 oligodendrocytes. In primary cultured OPCs, overexpression of Myt1L promoted, while knockdown inhibited OPC differentiation. Moreover, Myt1L was potently involved in promoting remyelination after lysolecithin-induced demyelination in vivo. ChIP assays showed that Myt1L bound to the promoter of Olig1 and transcriptionally regulated Olig1 expression. Taken together, our findings demonstrate that Myt1L is an essential regulator of OPC differentiation, thereby supporting Myt1L as a potential therapeutic target for demyelinating diseases.
Animals ; Cell Differentiation ; physiology ; Demyelinating Diseases ; chemically induced ; Lysophosphatidylcholines ; toxicity ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins ; metabolism ; Oligodendrocyte Precursor Cells ; cytology ; metabolism ; Oligodendroglia ; cytology ; metabolism ; Remyelination ; physiology ; Transcription Factors ; metabolism

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.

Objective To observe the effects of warm water bath active rewarming and passive rewarming on lung pathological injury and arterial blood gas of SD rats with hypothermia induced by prolonged seawater immersion.Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group (without any treatment) and the hypothermia group (seawater immersion at 20 ℃ for 24 h),The animals in the passive rewarming groups 1,2,3 and 4,each consisting of 10,had seawater immersion at 20 ℃for 24 h and received passive rewarming,and then they were respectively executed at 0,3,6 and 12 hours after rewarming,The animals in the active rewarming groups 1,2,3 and 4,each consisting of 10,underwent seawater immersion at 20 ℃ for 24 h and received active rewarming,and then they were sacrificed at 0,3,6and 12 hours after rewarming,Changes in lung pathology,arterial blood gas and other indicators were detected in all the animal groups.Results Both warm water bath active rewarming and passive rewarming all could help to restore lung injury and blood gas abnormality in rats with hypothermia induced by prolonged seawater immersion.Compared with that of the passive rewarming group [6 h:(7.6 ± 2.2) scores,12 h:(5.3 _± 1.3)scores],the recovery of lung pathological injury in warm water bath rewarming group was obviously better at 6 h(5.8 ± 1.2) scores and 12 h(3.8 ± 1.4) scores after rewarming,with statistical significance (P ＜ 0.05),and actual bicarbonate recovery was even better at 6 h after rewarming,also with statistical significance (P ＜0.05).Conclusions Compared with passive rewarming,warm water bath rewarming could significantly alleviate lung injury and arterial blood gas abnormality in hypothermic rats induced by prolonged seawater immersion,and it might produce even better effect on the prevention of rewarming-related acute respiratory distress syndrome.

Objective To investigate the dynamic changes in the nature of the pleural effusion via Light criteria in hypothermic rats induced by seawater immersion and analyze possible mechanism involved.Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group (without any treatment) and hypothermia group exposed to 20 ℃ seawater for 24 hours.Then,the hypothermia group was sub-divided into the passive rewarming groups 1,2,3 and 4 and warm water bath active rewarming groups 1,2,3 and 4,each consisting of 10 animals.The passive rewarming groups had passive rewarming after exposure to 20 ℃ seawater for 24 hours,while the active rewarming groups had warm water bath rewarming following exposure to 20 ℃ seawater for 24 hours.Then,all the animals in the sub-groups were executed 0,3,6 and 12 hours after rewarming.Serum,pleural effusion,total protein (TP) in pleural effusion,concentrations of lung homogenate lactate dehydrogenase (LDH) were measured,and Light criteria were calculated.Results There was no significant pleural effusion in the normal rats.LDH level in hypothermia-induced pleural effusion was higher than that in normal serum LDH,pleural effusion/total serum protein ratio (TPR) was lower than 0.5,and lactate dehydrogenase ratio (LDHR) was lower than 0.6.After rewarming,the amount of hypothermia-induced pleural effusion decreased gradually,while the levels of TPR and LDHR increased gradually.However,changes of LDH in pleural effusion were different with those in serum and lung homogenate.The warm water bath rewarming in the absorption of hypothermic pleural effusion was faster than passive rewarming,Warm water bath rewarming seemed to promote absorption of hypothermia-induced pleural effusion,but without statistical significance.Conclusions The 3 values of the pleural effusion criteria in hypothermic rats continuously increased following rewarming and reached the standards of effusion fluid,which did not necessarily reflect the seriousness of inflammatory pleural damage.The possible mechanism involved might be associated with the decrease of pleural effusion after rewarming,and water absorption by the body might be greater than protein absorption.

Objective To study the effects of active rewarming and passive rewarming on pulmonary oxidative stress and inflammatory response in rats with hypothermia induced by acute severe seawater immersion.Methods Sixty-four male healthy SD rats were randomly divided into the normal control group , the low temperature immersion group , the active rewarming group and the passive rewarming group . In accordance with rewarming time points , the two rewarming groups were further subdivided into the 2 h, 6 h and 12 h rewarming groups , each consisting of 8 animals.Effects of 2 different rewarming methods on lung oxygen free radicals ( MDA, SOD, GSH-PX) and serum inflammatory factors ( IL-6, IL-1β, TNF-a) were compared between the groups.Results (1) The MDA level [(2.84 ±0.46) nmol/mg pro] of the lungs in the 2 h active rewarming group was significantly higher than that of the 2 h passive rewarming group (P<0.05), and the MDA levels [(1.98 ±0.35) nmol/mg pro, (1.84 ±0.38) nmol/mg pro] of the 6 h and 12 h passive rewarming groups were slightly higher than those [(1.68 ±0.19) nmol/mg pro,(1.54 ±0.17) nmol/mg pro] of the 6 h and 12 h passive rewarming groups (P<0.05).(2) The SOD activity in the lungs of the 2 h and 6 h active rewarming groups was slightly higher than that of the 2 h and 6 h passive rewarming groups(P>0.05). The SOD activity in the lungs of the 12 h active rewarming group was higher than that of the 12 h passive rewarming group(P>0.05).(3) The GSH-PX activity in the lungs of the 2 h active rewarming group was slightly higher than that of the 2 h passive rewarming group(P>0.05).The GSH-PX activity in the lungs of the 6 h and 12 h active rewarming group was significantly higher than that of the 6 h and 12 h passive rewarming group(P<0.05).(4) The serum IL-1βand IL-6 levels of the 2 h passive rewarming group were obviously higher that those of the 2 h active rewarming group(P<0.05).The serum IL-1βand IL-6 levels in the 6 h and 12 h passive rewarming groups were slightly higher than those of the 6 h and 12 h active rewarming groups ( P<0.05).(5) The serum TNF-a levels of the 2 h, 6 h and 12 h passive rewarming groups were slightly higher that those of the 2 h, 6 h and 12 h active rewarming groups (P<0.05).Conclusion As compared with the active rewarming group , the activation of oxidative stress and inflammatory response in the passive rewarming group might worsen pulmonary lesion of the rats with hypothermia induced by acute severe seawater immersion .

Objective To establish hypothermia SD rat model induced by prolonged seawater immersion and to observe pathological damage to vital organs as well as certain important hematological parameters .Methods Twenty male adult Sprague-Dawley rats were randomly and equally divided into the normal control group and the hypothermia experimental group ( or simply the hypothermia group ) , each consisting of 10 rats.The control group was left there without any treatment , while the hypothermia group was immersed in artificial seawater at 20 ℃ for 24 hours to observe changes in vital signs of the rats during cold seawater immersion .At the end of the experiment , body temperature , general hematological parameters and pathological changes of vital organs were detected for further study .Results During the course of cold seawater immersion, the vital signs of the rats in the hypothermia group gradually worsened [( Heart rate before immersion (369 ±25.1) beats/min] vs (126.5 ±8.6) beats/min after immersion] (P<0.05).Respiratory rate before immersion was (92.8 ±7.2) times/min vs (43.9 ±3.8) times/min after immersion (P<0.05). Rectal temperature before immersion was (37.3 ±0.3) ℃vs (21.9 ±0.8) ℃ after immersion (P<0.05). After immersion, the blood routine detection indicated that hemoglobin level of the normal control group was (145.4 ±11.5) g/L, while that of the hypothermia group was (129.5 ±12.1) g/L ( P<0.05); neutrophil percentage of the normal control group was (18.3 ±3.5) ％, while that of the hypothermia group was (34.9 ± 6.1) ％(P<0.05).Prothrombin time (PT) of the normal control group was (11.42 ±2.36) s, while that of the hypothermia group was (17.86 ±2.41) s (P<0.05); APTT of the normal control group was (12.97 ± 2.41) s while that of the hypothermia group was (17.28 ±2.33) s (P <0.05).As for biochemical parameters, alanine aminotransferase (ALT) of the normal control group was (70.40 ±15.48) U/L, while that of the hypothermia group was (183.00 ±61.62) U/L (P<0.05); aspartate transaminase (AST) of the normal control group was (115.1 ±14.8) U/L, while that of the hypothermia group was (722.3 ±248.2) U/L (P<0.05);blood urea nitrogen (BUN) of the normal control group was (9.08 ±2.44) mmol/L, while that of the hypothermia group was (21.45 ±3.43) mmol/L (P<0.05);creatinine of the normal control group was (24.71 ±6.27) μmol/L, while that of the hypothermia group was (28.08 ±5.19) μmol/L (P<0.05);CK-MB of the normal control group was (451.00 ±266.53) U/L, while that of the hypothermia group was (2854.4 ±1089.6) U/L, with significant differences (P<0.05).Pathological detection indicated that there were lesions to various extents in all the vital organs , with the lesions to the lungs and stomach being most serious, and pleural effusion induced by hypothermia was also present .Conclusion The SD rat model of hypothermia induced by prolonged seawater immersion was successfully established for subsequent studies .Our present study showed that lungs and stomach were important target organs involved in prolonged seawater immersion.

Objective To observe changes in blood biochemistry and coagulation function before and after warm water bath rewarming in SD rats with hypothermia induced by prolonged seawater immersion . Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group ( the NC group, without any treatment ) and the hypothermia group ( the HT group, exposed to seawater immersion at 20 ℃for 24 hours).The passive rewarming sub-groups (the pR group 1, 2, 3 and 4, n=10) (exposed to seawater immersion at 20 ℃for 24 hours +passive rewarming ) were respectively executed after rewarming at hour 0, hour 3, hour 6, and hour 12).The warm-water bath rewarming sub-groups (the wR group 1, 2, 3 and 4, n=10 ) ( exposed to seawater immersion at 20 ℃ for 24 hours +warm-water bath rewarming ) were respectively executed after rewarming at hour 0, hour 3, hour 6, and hour 12).Blood samples were taken from abdominal aorta for biochemical and coagulation detection .Results Zero to 3 hours after warm water bath rewarming , important parameters of hepatic and renal functions , as well as myocardial enzymes in the SD rats with hypothermia induced by prolonged seawater immersion remained at high levels or even increased to some extent.Only after 6 hours after rewarming , the above-mentioned parameters dropped considerably .However, coagulation indicators began to decline immediately after rewarming , and as compared with the passive rewarming , warm water bath rewarming could produce obviously better effects on the alleviation of abnormal hepatic and renal functions, as well as myocardial enzyme parameters (P<0.05).Conclusion Warm water bath rewarming could produce better effects on the recovery of serum biochemical parameters in rats with hypothermia induced by prolonged seawater immersion when compared with those of passive rewarming .

Objective To observe the effects of warm water bath active rewarming and passive rewarming on lung pathological injury and arterial blood gas of SD rats with hypothermia induced by prolonged seawater immersion.Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group (without any treatment) and the hypothermia group (seawater immersion at 20 ℃ for 24 h),The animals in the passive rewarming groups 1,2,3 and 4,each consisting of 10,had seawater immersion at 20 ℃for 24 h and received passive rewarming,and then they were respectively executed at 0,3,6 and 12 hours after rewarming,The animals in the active rewarming groups 1,2,3 and 4,each consisting of 10,underwent seawater immersion at 20 ℃ for 24 h and received active rewarming,and then they were sacrificed at 0,3,6and 12 hours after rewarming,Changes in lung pathology,arterial blood gas and other indicators were detected in all the animal groups.Results Both warm water bath active rewarming and passive rewarming all could help to restore lung injury and blood gas abnormality in rats with hypothermia induced by prolonged seawater immersion.Compared with that of the passive rewarming group [6 h:(7.6 ± 2.2) scores,12 h:(5.3 _± 1.3)scores],the recovery of lung pathological injury in warm water bath rewarming group was obviously better at 6 h(5.8 ± 1.2) scores and 12 h(3.8 ± 1.4) scores after rewarming,with statistical significance (P ＜ 0.05),and actual bicarbonate recovery was even better at 6 h after rewarming,also with statistical significance (P ＜0.05).Conclusions Compared with passive rewarming,warm water bath rewarming could significantly alleviate lung injury and arterial blood gas abnormality in hypothermic rats induced by prolonged seawater immersion,and it might produce even better effect on the prevention of rewarming-related acute respiratory distress syndrome.