Objective To investigate the curative effect of acute severe brain injury complicated ARDS, Methods 31 patients who had acute severe brain injury complicated ARDS were divided into two groups:A group was early discovery of ARDS and given treatment.B group was late discovery of ARDS and treated late.Then the curative effects were compared.Results A group was significantly higher than B group in blood gas analysis(P

OBJECTIVETo investigate the importance of breastfeeding in preterm infants with various gestational ages.

METHODSA total of 639 preterm infants with a gestational age of 28-36weeks were enrolled, and according to the feeding pattern, they were divided into exclusive breastfeeding group (n=237) and formula milk feeding group (fed with liquid milk for preterm infants; n=402). These two feeding patterns were compared in terms of their effects on weight gain, laboratory markers including albumin (Alb) and alkaline phosphatase (ALP), incidence rate of feeding intolerance, and incidence rates of complications including necrotizing enterocolitis (NEC) and retinopathy of prematurity (ROP).

RESULTSCompared with the formula milk feeding group, the breastfeeding group had a significantly faster increase in body weight, a significantly lower incidence rate of NEC, a significantly higher ALP level, and a significantly lower Alb level in the preterm infants with a gestational age of 28-30 weeks (P<0.05); there were no significant differences between the two groups in the incidence rates of anemia, ROP, bronchopulmonary dysplasia (BPD), and nosocomial infection and length of hospital stay (P>0.05). For the preterm infants with a gestational age of 31-33 weeks, the breastfeeding group had a significantly faster increase in body weight, a significantly lower incidence rate of feeding intolerance, a significantly shorter length of hospital stay, and a significantly higher ALP level (P<0.05); there were no significant differences between the two groups in the incidence rates of NEC, anemia, ROP, BPD, and nosocomial infection and the Alb level (P>0.05). For the preterm infants with a gestational age of 34-36 weeks, there were no significant differences in these indices between the two groups (P>0.05).

CONCLUSIONSBreastfeeding plays an important role in increasing body weight, reducing the incidence rates of feeding intolerance and NEC, and shortening the length of hospital stay in preterm infants with a gestational age of 28-33 weeks.

Breast Feeding ; Bronchopulmonary Dysplasia ; etiology ; Enterocolitis, Necrotizing ; etiology ; Humans ; Infant Formula ; Infant, Newborn ; Infant, Premature ; Intensive Care Units, Neonatal ; Retinopathy of Prematurity ; etiology

Arteries in vivo are subjected to lumen pressure, shear flow and axial tension due to surrounding tissue tethering. The axial stress affects arterial function including its response to pressure and flow. While the effects of blood pressure and shear flow are well documented, the effects of axial tension on vascular remodeling have just gradually gained attention recently. This review summarizes the results on the observation of the axial tension in arteries and responses of arteries to elevation and reduction of the axial stress. It is concluded that the axial tension in arteries plays an important role in regulating normal arterial function and tissue remodeling and adaptation and disease development. Research on vascular remodeling under axial tension shall strengthen the understanding of normal physiological functions and pathological changes of the arteries.

Blood vessels are often subjected to axial torsion (or twist) due to body movement or surgery. However, there are few studies on blood vessel under twist. This review first summarizes the clinical observation on the twist of blood vessels and then presents what we know about the mechanical behaviors of blood vessel under twist, including the constitutive models. The state of art researches on the remodeling of blood vessels under twist via ex vivo organ culture, in vivo animal experiments, and mathematical model simulations are further discussed. It is our hope that this review will draw attention for further in-depth studies on the behavior and remodeling of blood vessels under twist.

Objective To study the mechanisms of vascular remodeling induced by hypertension and/or low shear stress, which will be helpful in the prevention, diagnosis and treatment of cardiovascular diseases. Method The models of low shear stress in carotid artery or of hypertension were established by the ligation of partial distal branches of the left common carotid artery (LCA) or by the coarctation of aorta in SD rats, respectively. For some rats, the low shear stress in LCA was accompanied by the hypertension. The wall thickness and the ratio of wall thickness to inner diameter were determined by morphometrical approach. The MMP-2 activity was detected by gel zymography, and the expression of proteins, including p-Akt, Rho GDIα, was verified by Western blotting in LCA. Results When LCA was subjected to hypertension or low shear stress, MMP-2 activity, the wall thickness, and the ratio of wall thickness to inner diameter were all increased significantly. They were further enhanced when the hypertension and low shear stress were both existed, which would speed the vascular remodeling. Low shear stress induced the expression of p Akt, and the lower shear stress, the higher p-Akt expression would be. However, the highest expression of p-Akt was observed in LCA of hypertension accompanied by low shear stress. The expression of Rho GDIα was upregulated in LCA by either low shear stress or hypertension. The highest expression of Rho GDIα was observed in LCA of hypertension accompanied by low shear stress. Conclusions Vascular remodeling could be mostly influenced in LCA subjected to low shear stress accompanied by hypertension, which was also regulated through the changing expression of p-Akt and Rho GDIα.

Objective To investigate the role of receptor for activated C kinase 1 (RACK1) in vascular smooth muscle cells (VSMCs) proliferation modulated by co-cultured endothelial cells (ECs) and shear stress. Methods Using EC/VSMC co-cultured parallel plate flow chamber system, two levels of shear stress, i.e. low shear stress (LowSS, 0.5 Pa) and normal shear stress (NSS, 1.5 Pa), were applied for 12 h. BrdU ELISA was used to detect the proliferation of VSMCs, and Western blot was used to detect the protein expressions of RACK1 and phosphor-Akt. Under the static condition, RNA interference was used to suppress the expression of RACK1 in VSMCs, and then the proliferation of VSMCs and expressions of RACK1 and phosphor-Akt were detected. By using co-culture model (ECs/VSMCs) and separated culture model (ECs//VSMCs), the effect of ECs on expressions of RACK1 and phosphor-Akt in VSMCs was further analyzed. Results Comparative proteomic analysis revealed that LowSS increased the expression of RACK1 in rat aorta. In vitro experiments showed that LowSS induced the proliferation, expressions of RACK1 and phospho Akt in VSMCs co-cultured with ECs. Target RNA interference of RACK1 significantly decreased the proliferation of VSMCs, and the phosphorylation of Akt. In comparison with ECs//VSMCs (separated culture) group, the expression of RACK1 and phosphor-Akt were both up-regulated in the VSMCs co-cultured with ECs (ECs/VSMCs group). Conclusions The expression of RACK1 in VSMCs was modulated by shear stress and neighboring ECs, which might induce cellular proliferation via PI3K/Akt pathway. The investigation on VSMC proliferation and the involved biomechanical mechanism will contribute to understanding and help preventing the pathogenesis and progress of atherosclerosis.

Objective To investigate the role of pathologically increased-cyclic stretch in proliferation of vascular smooth muscle cells (VSMCs) during hypertension, and the effect of Forkhead box protein O1 (FOXO1) during this process. Methods Coarctation of abdominal aorta above kidney artery of rat was used as hypertensive animal model, and sham-operated animal as control. FX-4000 cyclic stretch loading system was used to apply 5% physiologically cyclic stretch and 15% pathologically cyclic stretch during hypertension on VSMCs in vitro. Western blot was used to reveal the expressions of FOXO1 and phosphor-FOXO1 in VSMCs, and BrdU kit to detect the proliferation of VSMCs in vitro. By using RNA interference in static, the role of FOXO1 on cell proliferation was further detected. Results After abdominal aorta coarctation for 2 and 4 weeks, respectively, the blood pressure was significantly increased compared with the sham operated rats. The proliferation of vascular cells in aorta of hypertensive rat was significantly increased, and so did the expressions of FOXO1 and phosphor-FOXO1. In vitro experiment revealed that 15% cyclic stretch remarkably increased the proliferation and expressions of FOXO1 and phospho FOXO1 in VSMCs. Target siRNA transfection in static decreased the expression of FOXO1 and phosphor-FOXO1, as well as the proliferation of VSMCs. Conclusions Pathologically increased-cyclic stretch may increase the expression and phosphorylation of FOXO1, subsequently modulate VSMC proliferation during hypertension. Based on animal models, this study intends to reveal the role of FOXO1 in vascular reconstruction of hypertension and the involved biomechanical mechanism, so as to make the mechanobiological mechanism of hypertension explicit and discover new target in the prevention and treatment of vascular remodeling.

Objective To study the role of cyclic strain-modulated tumor necrosis factor-α (TNF-α) played in the quantity and intercellular cell adhesion molecule-1(ICAM-1) expression of endothelial microparticles (EMPs). Methods The endothelial cells (ECs) primarily cultured from rat aorta were applied with 5% cyclic strain (to simulate normal physiological condition) and 18% cyclic strain (to simulate hyper-tension condition), respectively, by using FX-4000T cyclic stain loading system for 24 hours at the loading frequency of 1.25 Hz. The mRNA expression of TNF-α under different amplitudes of cyclic strain was determined by real time-PCR. The TNF-α was then used to stimulate the ECs from rat aorta, and the supernatants were collected and ultracentrifuged to get endothelial microparticles (EMPs), which were then identified by lipophilic styryl membrane staining and transmission electron microscope for morphological identification. The quantities of Annexin V positive EMPs under TNF-α stimulation were counted by flow cytometer and ICAM-1 expression on EMPs was detected as well. Results Compared with the 5% normal cyclic strain, under 18% high cyclic strain condition,the mRNA expression of TNF-α in ECs increased significantly. TNF-α could then significantly up-regulate the production of Annexin V positive EMPs and promote the expression of ICAM-1 on EMPs. Conclusions The over-expression of TNF-α in ECs under high cyclic strain might mediate the high production of EMPs and over-expression of ICAM-1 on EMPs. The research findings will provide new experiment evidence for further studying the role of EPCs in the mechanobiological mechanism of vascular remodeling.