Preterm birth (PTB), predominantly induced by intraamniotic inflammation, stands as the foremost contributor to neonatal morbidity and mortality globally. Fetal inflammatory response syndrome, stemming from the activation of the innate immune system, signifies the occurrence of funisitis or chorionic vasculitis. Maternal-fetal complications associated with infection-related PTB encompass maternal sepsis, fetal demise, neonatal sepsis, neonatal neurological impairment, and chronic lung disease. The inflammatory cascade is initiated when Toll-like receptors present on immune cells within the fetal membranes and the female reproductive tract encounter pathogen-associated molecular patterns derived from infectious agents. Subsequently, the nuclear factor kappa-light-chain-enhancer of activated B cells facilitates the transcription of cytokines. The accumulation of neutrophils compromises the tissue integrity of the fetal membranes, leading to membrane rupture via the secretion of matrix metalloproteinases. Elevated prostaglandin levels prompt uterine contractions and cervical remodeling, resulting in progressive cervical effacement and dilation, ultimately culminating in fetal delivery. The diagnosis of PTB should encompass three pivotal criteria: gestational age, uterine activity, and the consequences of that uterine activity. The diagnosis of chorioamnionitis is established through a combination of clinical manifestations, laboratory findings, identification of infectious microorganisms, and placental pathology. Fetal monitoring involves antenatal ultrasonography and non-stress testing. The management of infection-related PTB involves controlling and treating the infection, timing delivery to coincide with optimal fetal lung maturity, and optimizing outcomes for both the mother and neonate. Current preventive strategies for PTB primarily focus on inhibiting myometrial contractions that arise from the inflammatory cascade initiating PTB. An understanding of these pathways serves as the cornerstone for the development of therapeutic interventions aimed at preventing PTB.

Preterm birth (PTB), predominantly induced by intraamniotic inflammation, stands as the foremost contributor to neonatal morbidity and mortality globally. Fetal inflammatory response syndrome, stemming from the activation of the innate immune system, signifies the occurrence of funisitis or chorionic vasculitis. Maternal-fetal complications associated with infection-related PTB encompass maternal sepsis, fetal demise, neonatal sepsis, neonatal neurological impairment, and chronic lung disease. The inflammatory cascade is initiated when Toll-like receptors present on immune cells within the fetal membranes and the female reproductive tract encounter pathogen-associated molecular patterns derived from infectious agents. Subsequently, the nuclear factor kappa-light-chain-enhancer of activated B cells facilitates the transcription of cytokines. The accumulation of neutrophils compromises the tissue integrity of the fetal membranes, leading to membrane rupture via the secretion of matrix metalloproteinases. Elevated prostaglandin levels prompt uterine contractions and cervical remodeling, resulting in progressive cervical effacement and dilation, ultimately culminating in fetal delivery. The diagnosis of PTB should encompass three pivotal criteria: gestational age, uterine activity, and the consequences of that uterine activity. The diagnosis of chorioamnionitis is established through a combination of clinical manifestations, laboratory findings, identification of infectious microorganisms, and placental pathology. Fetal monitoring involves antenatal ultrasonography and non-stress testing. The management of infection-related PTB involves controlling and treating the infection, timing delivery to coincide with optimal fetal lung maturity, and optimizing outcomes for both the mother and neonate. Current preventive strategies for PTB primarily focus on inhibiting myometrial contractions that arise from the inflammatory cascade initiating PTB. An understanding of these pathways serves as the cornerstone for the development of therapeutic interventions aimed at preventing PTB.

BACKGROUND:C2 transpedicle screw fixation for Hangman fractures has been paid more attention due to reliability and no loss of physiological function.However,there are lacks of biomechanical evidences for indication treatment because the fixation is single segmental.OBJECTIVE:To investigate the biomechanical stability of C2 transpedicle screw fixation for Hangman fractures.DESIGN,TIME and SEITING:This was a contrast study which was performed at the General Key Laboratory of Biomechanics,First Military Medical University of Chinese PLA from May to August 2004.MATERIALS:AO-universal titanium alloy transpedicle screw of 18 25 mm in length and 3.5 mm in diameter was adopted in this study.Six fresh C1-C4 cervical vetebrae samples were ordiually made into type Ⅰ,ⅡA,and Ⅱ Hangman fracture models.METHODS:After transpedicle screw fixation.Hangman fracture models were measured by non-destroyed style with spinal anterior flexion/posterior extension,left/right lateral curvature,and left/right axial direction.Loading/unlonding circulation was performed three times during each testing.Kinematics indicators were measured on the 3rd circulation.MAIN OUTCOME MEASURES:Spinal motor images at zero load and maximal load were obtained with laser photoscanning(0.1% in precision),and the corresponding systematic software was adopted to calculate 3D range of movement.RESULTS:The relative stability of type Ⅰ Hangman fracture models after C2 transpedicle screw fixation was 100.62%(inflexion),96.91%(posterior extension),99.19%(lateral curvature),and 97.12%(rotation)as compared to control group (P＞0.05).The relative stability of type Ⅱ Hangman fracture models after C2 transpedicle screw fixation was 47.84%(inflexion),21.29%(posterior extension),65.98%(lateral curvature),and 41.69%(rotation)as compared to control group (P＜0.05).CONCLUSION:Biochemical evaluation suggests that type Ⅰ and Ⅱ A Hangman fractures do fit for C2 transpedicle screw fixation,and the fixation may generate well physiological fixation or stability.However,stability of type Ⅱ Hangman fracture is poor,so it is not suitably adopted single transpedicle screw fixation.

BACKGROUND: The rudiment of tissue engineering is to obtain tissue from patients. The cells are expanded into a population through cellular culture, and seeded into scaffolds, which can accommodate and guide the growth and proliferation of new cells in the three-dimensional scaffolds. At last, the constructed tissue is transplanted in vivo to repair or replace damaged or diseased tissues. Afterward neovascularization of the graft, the scaffolds are absorbed gradually. Finally, the new tissue replaces completely the damaged or diseased tissuesOBJECTIVE: To evaluate the feasibility of designing and fabricating customized anatomical-shaped bone tissue-engineering scaffolds with reverse engineering and rapid prototyping (RP) techniques. To avoid the disadvantage of the conventional fabricated methods of the scaffolds.DESIGN: The method of fabricating customized anatomical-shaped bone tissue engineering scaffolds.SETTING: Computer-aided design (CAD) of the scaffold was conducted in CAD training center, Guangdong Machinery Research Institute. Rapid prototyping fabrication of the scaffold was conducted in Guangdong Longchuangyu Limited Cooperation. The scaffold was fabricated by sterophotocureable technology and was made of photosensitized resin.METHODS: This experiment was carried out at the Center of Department of Traumatic Orthopedics, General Hospital of Guangzhou Military Area Command of Chinese PLA from October 2004 and January 2005. According to reverse engineering, layered image information of skeleton of the patients was scanned with CT/MRI. Anatomical models of region of interesting were created by means of CT or MRI three-dimensional reconstruction and surface reconstruction. The internal construction of the scaffolds was designed with CAD software in the outline of the anatomical models to develop computer-aided model. The prototypes of the scaffolds were fabricated by RP process.MAIN OUTCOME MEASURES: ①CT/MRI scanning, three-dimensional reconstruction, anatomical modeling; ② computer-aided design of customized bone tissue engineering scaffolds; ③rapid prototyping fabrication of customized bone tissue engineering scaffold.RESULTS: ①Anatomical models of bone joint were established through CT/MRI three-dimensional reconstruction. ② The internal structure of the scaffold was designed to establish the entity model of bone tissue engineering scaffold successfully with computer-aided design software. ③ CAD model of bone tissue engineering scaffold guided prototypes to develop the customized anatomical-shaped bone tissue engineering scaffolds. The internal structure of bone tissue engineering scaffold was fine and had high degree of porosity-and pore interconnectivity.CONCLUSION: Customized anatomical-shaped bone tissue engineering scaffolds can be fabricated with reverse engineering and RP technology. Among all RP processes, stereophotocureable technology (SLA) is the best one with good precision, smooth surface and good shaping.