Stability analysis of riverbanks with a dual structure under water-root-soil coupling.

The collapse mechanism of dual-structure vegetation riverbanks at different water levels is unclear. A method for calculating the critical collapse width of a dual-structure vegetation bank under different failure modes that consider the variations in river and groundwater levels and the influence of vegetation roots is proposed. Combined with the influence of flow lateral erosion and slope toe accumulation, a calculation model of riverbank stability was established. The results show that shear failure is the main failure mode when the cohesive soil layer on a dual-structure bank is thick, and the critical collapse width of the bank with root soil is higher than that of the soil bank. The critical collapse width of the bank varied with the water level during different water level periods. Compared with a soil riverbank, a rooted soil riverbank can significantly prolong the bank collapse time. The collapse width of a soil bank without vegetation roots is smaller than that of a rooted soil bank, and the cumulative collapse width is related to calculation time. The greater the thickness of rooted soil, the slower the decay rate of bank stability under water flow erosion.

Qiliqiangxin Attenuates Adverse Cardiac Remodeling after Myocardial Infarction in Ovariectomized Mice via Activation of PPARγ.

BACKGROUND/AIMS: This study was designed to investigate the therapeutic effect of traditional Chinese medication Qiliqiangxin (QLQX) on adverse cardiac remodeling after myocardial infarction (MI) in bilateral ovariectomized (OVX) female mice. METHODS: Eight-week old female C57BL/6 mice were operated to ligate the left anterior descending coronary artery seven days after bilateral ovariectomy and were orally administered either QLQX or vehicle. 21 days after ligation, echocardiography was performed to evaluate the heart function of all mice. Masson's Trichrome staining was applied to evaluate myocardial fibrosis. Collagen deposition was determined by the mRNA level of Collagen I, Collagen III and α-SMA using real-time quantitative polymerase chain reaction (qPCR). Myocardial apoptosis was examined by the protein level of Bax, Bcl2 and the Bcl2/Bax ratio using western blotting. RESULTS: These mice displayed a significant reduction in heart function, increased myocardial fibrosis and apoptosis, and decreased expression of peroxisome proliferator activated receptor γ (PPARγ) in the heart tissue, which could be reversed by QLQX treatment. Inhibition of PPAR reduced QLQX-mediated cardio-protective effects, while PPARγ activation did not further enhance the beneficial effect of QLQX. Furthermore, QLQX upregulated 9 genes (Cd36, Fatp, Pdk4, Acadm, Acadl, Acadvl, Cpt1a, Cpt1b and Cpt2) facilitating energy metabolism in the MI hearts of the OVX mice and 5 (Acadm, Acadl, Cpt1a, Cpt1b, Cpt2) of the 9 genes were the downstream targets of PPARγ. CONCLUSION: The present study indicates that QLQX has a treatment effect on pathological remodeling post MI in bilateral OVX female mice via activation of PPARγ, suggesting that QLQX may be a promising prescription for the treatment of postmenopausal women suffering from MI.

Traditional Chinese Medication Qiliqiangxin Protects Against Cardiac Remodeling and Dysfunction in Spontaneously Hypertensive Rats.

Qiliqiangxin (QLQX), a traditional Chinese herbs medication, exerted protective effect in chronic heart failure patients in a multicenter randomized double-blind study. QLQX has also been found to improve cardiac function and reduce cardiac fibrosis in spontaneously hypertension animal model. However, the effect of longterm treatment with QLQX in such a condition and the related molecular mechanisms remain largely unknown. In the present study, thirteen-week-old spontaneously hypertensive rats (SHRs) were treated by daily intragastric administration of QLQX or saline for one year. Echocardiography, electron microscopy, and Masson's trichrome staining were used to determine cardiac function, mitochondria ultrastructure, and cardiac fibrosis, respectively. Quantitative reverse transcription polymerase chain reactions (qRT-PCRs) and Western blotting were used to determine gene expressions. We found that QLQX significantly improved cardiac function and reduced gene markers of pathological hypertrophy including ANP, BNP, and Myh7. QLQX also attenuated cardiac fibrosis and apoptosis in SHRs as evidenced by downregulation of α-SMA, collagen I, collagen III, and TGF-ß expressions and reduction of Bax to Bcl-2 ratio. Moreover, the damage of mitochondrial ultrastructure was greatly improved and the reduction of PPAR-α, PPAR-γ, and PGC-1α expression levels was significantly restored in SHRs by treatment with QLQX. In conclusion, longterm treatment with QLQX protects against cardiac remodeling and dysfunction in hypertension by increasing PPARs and PGC-1α.

Estrogen Receptor α and ß in Mouse: Adipose-Derived Stem Cell Proliferation, Migration, and Brown Adipogenesis In Vitro.

BACKGROUND/AIMS: Adipose-derived stem cells (ASCs) belong to mesenchymal stem cells and may play a potential role as seeding cells in stem cell transplantation. To be able to exploit stem cells as therapeutic tool, their defects in some important cellular functions, such as low survival rate and cellular activity, should be considered. This is especially the case for stem cells that are intended for transplantation. Of note, stem cell responses to hormones should be considered since estrogen is known to play a critical role in stem cell behavior. However, different impacts of the estrogen receptor (ER) types α and ß have not been fully determined in ASC function. In this study, we investigated effects of ERα and ERß on ASC proliferation, migration, as well as in adipogenesis. METHODS: ASCs obtained from mice were cultured with 100nM ERα or ERß agonist PPT and DPN, respectively. The ERα and ERß antagonist ICI 182,780 (100nM) was used as control. RESULTS: Compared to ERß, ERα appears more potent in improving ASC proliferation and migration. Investigation of adipogenesis revealed that ERß played a significant role in suppressing ASC-mediated brown tissue adipogenesis which is in contrast to ERα. These results correlated with reduced mRNA expression of UCP-1, PGC-1α and PPAR-x03B3;. CONCLUSIONS: ERα plays a more critical role in promoting ASC proliferation and migration while ERß is more potent in suppressing ASC brown adipose tissue differentiation mediated by decreased UCP-1, PGC-1α and PPAR-x03B3; expression.

Cardioprotective activity of placental growth factor in a rat model of acute myocardial infarction: nanoparticle-based delivery versus direct myocardial injection.

BACKGROUND: To comparatively evaluate the cardioprotective activity of placental growth factor (PGF) delivered through direct injection and a nanoparticle-based system respectively and to study the underlying mechanisms in a rat model of acute myocardial infarction (AMI). METHODS: Poly lactic-co-glycolic acid (PLGA)-based PGF-carrying nanoparticles (PGF-PLGANPs) were created. The mean size and morphology of particles were analyzed with particle size analyzer and transmission electronic microscopy (TEM). Encapsulation efficiency and sustained-release dose curve were analyzed by ELISA. Sprague-Dawley rats were randomized into four groups (n = 10). While animals in the first group were left untreated as controls, those in the other 3 groups underwent surgical induction of AMI, followed by treatment with physiological saline, PGF, and PGF-PLGANPs, respectively. Cardiac function was evaluated by transthoracic echocardiography at 4 weeks after treatment. At 6 weeks, rats were sacrificed, infarction size was analyzed with Masson trichrome staining, and protein contents of TIMP-2, MT1-MMP and MMP-2 at the infarction border were determined by immunohistochemistry and western blotting analysis. RESULTS: PGF was released for at least 15 days, showing successful preparation of PGF-PLGANPs. Coronary artery ligation successfully induced AMI. Compared to physiological saline control, PGF, injected to the myocardium either as a nude molecule or in a form of nanoparticles, significantly reduced infarction size, improved cardiac function, and elevated myocardial expression of TIMP-2, MT1-MMP, and MMP-2 (P < 0.05). The effect of PGF-PLGANPs was more pronounced than that of non-encapsulated PGF (P < 0.05). CONCLUSION: Target PGF delivery to myocardium may improve cardiac function after AMI in rats. PLGA-based nanoparticles appear to be a better approach to delivery PGF. PGF exerts its cardioprotective effect at least partially through regulating metalloproteinase-mediated myocardial tissue remodeling.

Comparison of the safety of right internal mammary artery versus radial artery for the second arterial conduit during coronary artery bypass grafting.

OBJECTIVE: To compare the safety of procedure in patients receiving right internal mammary artery (RIMA) versus radial artery (RA) as the second arterial graft during left internal mammary artery bypass surgery. METHODS: A literature search was performed, and observational studies comparing RA and RIMA as a second arterial conduit were included. The end points included in-hospital mortality, sternal wound infection (SWI), myocardial infarction (MI), reoperation for bleeding, stroke and low cardiac output syndrome. Sensitivity analysis was performed, and publication bias was assessed. RESULTS: Analysis of nine studies comprising 1,738 RIMA patients and 1,906 RA patients showed a similar risk of in-hospital mortality (relative risk [RR] 1.13, 95% confidence interval [CI] 0.64 to 1.98) between two groups. The risk of SWI in RIMA patients was significantly higher than that in RA patients (RR 3.19, 95% CI 1.64 to 6.20). The risk of the rest end points did not differ. CONCLUSIONS: The postoperative risk seems to be similar between RIMA group and RA group, except the higher risk of SWI in RIMA patients. The surgeon relies on his own experience with these two arterial grafts and assessment of the patient profile to decide the choice of the second arterial conduit.

Integrated bulk and single-cell RNA sequencing identifies an aneuploidy-based gene signature to predict sensitivity of lung adenocarcinoma to traditional chemotherapy drugs and patients' prognosis.

Background: Patients with lung adenocarcinoma (LUAD) often develop a poor prognosis. Currently, researches on prognostic and immunotherapeutic capacity of aneuploidy-related genes in LUAD are limited. Methods: Genes related to aneuploidy were screened based on bulk RNA sequencing data from public databases using Spearman method. Next, univariate Cox and Lasso regression analyses were performed to establish an aneuploidy-related riskscore (ARS) model. Results derived from bioinformatics analysis were further validated using cellular experiments. In addition, typical LUAD cells were identified by subtype clustering, followed by SCENIC and intercellular communication analyses. Finally, ESTIMATE, ssGSEA and CIBERSORT algorithms were employed to analyze the potential relationship between ARS and tumor immune environment. Results: A five-gene ARS signature was developed. These genes were abnormally high-expressed in LUAD cell lines, and in particular the high expression of CKS1B promoted the proliferative, migratory and invasive phenotypes of LUAD cell lines. Low ARS group had longer overall survival time, higher degrees of inflammatory infiltration, and could benefit more from receiving immunotherapy. Patients in low ASR group responded more actively to traditional chemotherapy drugs (Erlotinib and Roscovitine). The scRNA-seq analysis annotated 17 cell subpopulations into seven cell clusters. Core transcription factors (TFs) such as CREB3L1 and CEBPD were enriched in high ARS cell group, while TFs such as BCLAF1 and UQCRB were enriched in low ARS cell group. CellChat analysis revealed that high ARS cell groups communicated with immune cells via SPP1 (ITGA4-ITGB1) and MK (MDK-NCl) signaling pathways. Conclusion: In this research, integrative analysis based on the ARS model provided a potential direction for improving the diagnosis and treatment of LUAD.

MRI pathoanatomy study of congenital vertical talus.

BACKGROUND: Prior reports regarding the pathologic anatomy for congenital vertical talus have noted some disagreement as to which elements of the pathologic anatomy are consistently present. The purpose of his study is to evaluate the 3-dimensional morphologic changes and pathoanatomy of the congenital vertical talus using magnetic resonance imaging. METHODS: Nine patients with congenital vertical talus (ranging from 5 mo-11 y) underwent magnetic resonance imaging of both feet. A foot and ankle coil was used for the 1.5 T system. The protocol consisted of T1-weighted spin echo sequence image and T2-weighted fast spin echo sequence image in the sagittal, coronal, and axial planes. Slice thickness ranged from 3 to 4 mm with 0 to 1.0 mm interspace thickness. A descriptive analysis was performed based upon the T1-weighted image by physicians. RESULTS: At the level of the talonavicular joint, the navicular was seen significantly subluxed dorsally with associated wedging of the navicular. At the level of the calcaneocuboid joint, often there was a significant dorsal subluxation of the cuboid in relation to the calcaneus. Lateral obliquity of the calcaneocuboid joint could be present to varying degrees. The anterior calcaneus was significantly laterally displaced in relation to the talar head with an element of lateral translation and eversion of the calcaneus at the subtalar joint. Distal cavus at the cuneiform-first metatarsal joint was observed in 5 patients. CONCLUSIONS: This study suggests that there is significant pathology at the level of subtalar joint in congenital vertical talus. In addition to satisfactory reduction of the talonavicular joint, methods to ensure realignment of the calcaneus under the talus may be a crucial component of deformity correction and to prevent recurrence of deformity. LEVEL OF EVIDENCE: A Level III diagnostic study using normal pediatric foot anatomy in magnetic resonance imaging as a reference.

Molecular cloning and sequence analysis of Spot 14 alpha in geese.

1. Spot 14 alpha acts as a transcription factor involved in the regulation of adipogenic enzymes via three thyroid response elements in its promoter region. The objective of the current research was to clone and sequence the Spot 14 alpha gene in geese. 2. We cloned the cDNA sequence of goose Spot 14 alpha. The gene was predicted to encode a peptide of 128 amino acids, which has sequence identities of 87% cDNA and 84% amino acids, with the duck counterparts. High percentages of G and C nucleotides were found in exon and 3' untranslated region of the goose Spot 14 alpha cDNA. 3. A novel frameshift mutation that leads to a damaged leucine zipper motif was observed at nucleotide position 399-400. This can influence the homodimerisation of Spot 14 alpha, probably resulting in dysfunction in the Spot 14 family in vivo. 4. Phylogenetic analysis revealed that goose and duck Spot 14 alpha form a monophyletic group. The Spot 14 alpha mRNA was highly expressed in the liver and adipose tissue of geese. The mRNA concentration and polymorphism of Spot 14 alpha in the lipogenic tissues of geese were related to the fatness trait.

REV3L, the catalytic subunit of DNA polymerase ζ, is involved in the progression and chemoresistance of esophageal squamous cell carcinoma.

Protein reversionless 3-like (REV3L), the catalytic subunit of DNA polymerase (pol) ζ, is well known to participate in error-prone translesion synthesis (TLS) with less stringent and lower processivity. Recent evidence has demonstrated that REV3L is involved in carcinogenesis and tumor progression. However, the function of REV3L remains unclear in esophageal squamous cell carcinoma (ESCC). In the present study, we examined REV3L expression in ESCC tissues and its association with clinicopathological parameters. REV3L was found to be significantly upregulated and correlated with lymph node metastasis and clinical stage in the ESCC tissues. To further investigate the potential role of REV3L in esophageal cancer, stable ESCC cell lines with suppression of REV3L expression were established. Downregulation of REV3L expression led to a decrease in cell proliferation and invasive capacity partly through suppression of cyclin D1 and survivin expression, and an increase in cellular sensitivity to 5-fluorouracil (5-FU) by induction of G1 phase arrest and apoptosis. Therefore, REV3L plays an important role in ESCC progression and chemoresistance, and is a potential diagnostic marker and therapeutic target for ESCC.

Correlation Between the Expression of MicroRNA-301a-3p and the Proportion of Th17 Cells in Patients with Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is characterized by chronic synovial inflammation and subsequent joint destruction. Previous studies have confirmed that Th17 cells play a critical role in the pathogenesis of RA. MicroRNA (miR)-301a-3p is a regulatory factor for Th17 cells differentiation that contributes to the pathogenesis of autoimmune diseases. The purposes of this study were to identify the alteration of Th17 cells and analyze the correlation between the expression of the miR-301a-3p and the proportion of Th17 cells in RA patients. The results showed that the frequency of Th17 cells and the expression of transcription factors (RORγt and STAT3) significantly increased in the peripheral blood mononuclear cells (PBMCs) from RA patients, and the associated proinflammatory cytokines were also upregulated. We also observed that the expression of protein inhibitor of activated STAT3 (PIAS3), the main cellular inhibitor of STAT3, was attenuated in RA patients and negatively correlated with the percentage of Th17 cells in RA. Interestingly, miR-301a-3p, an inhibitor of PIAS3 expression, was overexpressed in the PBMCs from RA patients and positively correlated with the frequency of Th17 cells in patients with RA. Taken together, these data indicated that miR-301a-3p and Th17 cells were augmented in peripheral blood, which may play an important role in the process of RA.

Affects of different access routes on autologous satellite cell implantation stimulating myocardial regeneration.

OBJECTIVE: To study the effect of different access routes on autologous satellite cell implantation to stimulate myocardial regeneration. METHODS: Satellite cells were procured from skeletal muscle (gluteus max) of adult mongrel canine, cultured, proliferated and labeled with 4', 6-diamidino-2-phenylindone (DAPI) in vitro. The cells were autologously implanted into the site of acute myocardial infarction by local injection or perfusion through the ligated distal left anterior descending coronary artery. Specimens were harvested 2, 4 and 8 weeks later for histological study. RESULTS: The labeling efficiency of satellite cells with DAPI was close to 100%. Fluorescent cells were found at the infarcted zone, papillary muscle and local injection site. Some of these cells had progressively differentiated into striated muscle fibers connected to intercalated discs. The infant cells appeared different from the mature myocardium under an electron microscope. Satellite cells implanted by perfusion through the coronary artery were arranged in order of consistency with host myocardial fibers. The satellite cells, implanted by local injection, were found growing in a disordered way. CONCLUSION: Satellite cells, implanted by coronary artery perfusion, can progressively differentiate into striated muscle fibers, arranging in order and disseminating over the infarcted zone. This approach seems more favorable for the recovery of myocardial contractile function than that of local injection.

Influence of skeletal muscle satellite cells implanted into infarcted myocardium on remnant myocyte volumes.

OBJECTIVE: To study the effects of skeletal muscle satellite cells implanted into infarcted myocardium on the volume of remnant myocytes. METHODS: Thirty-six adult mongrel canines were divided randomly into implantation group and control group. In the implantation group, skeletal muscle satellite cells taken from the gluteus maximus muscles of the dogs were cultured, proliferated and labeled with 4',6-diamidino-2-phenylindone (DAPI) in vitro. In both groups, a model of acute myocardial infarction was established in every dog. In the implantation group, each dog was injected with M199 solution containing autologous skeletal muscle satellite cells. The dogs in the control group received M199 solution without skeletal muscle satellite cells. The dogs of both groups were killed 2, 4 and 8 weeks after implantation (six dogs in a separate group each time). Both infarcted myocardium and normal myocytes distal from the infracted regions isolated were observed under optical and fluorescent microscope. Their volumes were determined using a confocal microscopy image analysis system and analyzed using SAS. A P < 0.05 was considered significant. RESULTS: A portion of the implanted cells differentiated into muscle fiber with striations and were connected with intercalated discs. Cross-sectional area and cell volume were increased in normal myocardium. Hypertrophy of remnant myocytes in the infarcted site after skeletal muscle cell implantation was much more evident than in the control group. Cross-sectional area, cell area and cell volume differed significantly from those of the control group (P < 0.05). Hypertrophy of the cells occurred predominantly in terms of width and thickness, whereas cell length remained unchanged. CONCLUSION: Skeletal muscle satellite cells implanted into infarct myocardium, could induce the hypertrophy of remnant myocyte cells in the infarcted site and could also aid in the recovery of the contractile force of the infarcted myocardium.

Bacterial growth characteristics in craniocerebral gunshot wound of cat in a hot and humid environment.

OBJECTIVE: To investigate the growth behavior of characteristics in craniocerebral gunshot wound of cats in a hot and humid environment. METHODS: Twenty-three cross-bred cats were randomly divided into 4 groups: group A, the gunshot wound control group at normal temperature, in which tissue sampling was performed immediately after the wounding; group B, another gunshot wound control group at normal temperature, in which the samples were taken 6 h after the wounding; group C, the gunshot wound group subjected to a hot and humid environment, in which the tissue samples were obtained 6 h after the wounding; group D, the control group without undergoing the wound. The tissues from the wound tract and the surrounding tissues were sampled for bacterial culture and counting. RESULTS: The bacterial counts of the tissues from the wound tract, the tissues within 5 mm and within 5-10 mm from wound tract varied insignificantly between groups A, B and C (P>0.05). In each group, the bacterial counts declined in the tissues as the distance of the sampling sites from the wound tract increased (P<0.01). The bacterial counts of the tissues from the wound tract and within 5 mm from the wound tract in group A, B and C were significantly different from those in group D (P<0.01). CONCLUSION: Hot and humid environment does not significantly affect the bacterial growth in the craniocerebral gunshot wound within the first 6 h, which is a safe period against rapid bacterial growth and suitable for debridement.

[Pathological changes of cat brain tissues after cranial gunshot wound in hot and humid environment].

OBJECTIVE: To investigate pathological changes in cat brain tissues after gunshot wound in the head in hot and humid environments. METHODS: Sixteen cats were randomly divided into 4 groups, namely the normal environment (group 1), gunshot in normal environment (group 2), hot and humid environment (group 3), and gunshot wound in hot and humid environment (group 4) groups. Pathological changes of the cat brain tissues were observed with both optical and electron microscopes. RESULTS: The early-stage changes in group 2 were high-lighted by vasomotor dysfunction, with the coexistence of both vascular spasm and dilation. In group 3, vascular spasm was depressed while hemorrhagic changes increased. On the brain tissue sections in group 4 for optical microscopic observation and ultra-thin sections for electron microscopic examination, the number of viable neural cells was obviously reduced, and edema, degeneration of the organelle occurred; loosening of the capillary tight junction, rupture and bleeding of the blood vessels, as well as degeneration and loosening of the myelin sheath were observed by transmission and scanning electron microscopes, and such changes were more serious than those in group 2. CONCLUSION: The hot and humid environment can significantly affect the pathological changes in the brain tissues of cat with cranial gunshot wound.

[Changes of cat cerebral microcirculation and blood-brain barrier in early stage of craniocerebral gunshot wound in the hot and humid environment].

OBJECTIVE: To study the changes of cat cerebral microcirculation in early stage after craniocerebral gunshot wound in the hot and humid environment to provide laboratory evidence for clinical treatment of such wound. METHODS: Craniocerebral gunshot wound was induced in 24 cats according to the method described by Carey with modifications, and the cats were placed in a cabin with environmental temperature and humidity of 25 degrees Celsius and 50% (group A), and 35 degrees Celsius and 85% (group B), respectively, to observe the changes in all the indices of cerebral microcirculation. RESULTS: All the cats survived and notable changes occurred in the morphology and permeability of cerebral microvascular along with obvious pathological changes in the brain tissue, and the vital signs, hemorheology and blood-brain barrier were significantly different between groups A and B. CONCLUSION: Hot and humid environment induces obvious changes in cat cerebral microcirculation and blood-brain barrier function in the early stages after craniocerebral gunshot wound.

[Establishment of canine models of penetrating craniocerebral gunshot wound].

OBJECTIVE: To establish a canine model of penetrating craniocerebral gunshot wound. METHOD: Gunshot wound was induced in 54 cross-bred dogs using 7.62-mm pistol bullets fired using a pistol from a distance of 30 cm in coronal direction with a tilt of 10 degrees toward the orbit, causing penetrating craniocerebral injury 1 cm posterior and 1.5 cm superior to the lateral canthus. The breathing and pathological changes in the brain tissue were observed after the injury. RESULTS: Autonomous breathing was recovered in 9 out of 21 dogs with respiratory arrest after the injury, and the total survival rate was 77.8% in the 54 dogs after the injury. Intracranial hematoma, intracranial pneumatosis, contusion and laceration of brain, and cranial bone fragments were found by cranial CT, with the entrance and exit of the bullet seen on the right and left frontal bone respectively. Pathological examination showed contusion and laceration of the brain tissues. CONCLUSION: The model of craniocerebral perforating wound has been successfully established in dogs.

[Construction and application of a lentiviral vector of single-chain variable fragment antibody against human hepatocyte growth factor receptor].

OBJECTIVE: To construct a lentiviral expression vector carrying the single-chain variable fragment (scFv) antibody against human hepatocyte growth factor receptor (HGFR), express it in transfected HEK293 cells, and observe its biological function of specific binding to antigen. METHODS: The variable regions of the heavy chain (VH) and light chain (VL) genes were amplified directly from the cDNA of hybridoma cell line 8E8 secreting mouse anti-human HGFR antibody and assembled using the splice overlap extension-PCR (SOE-PCR). The constructed HGFR-scFv gene with the signal peptide SP-VH-linker-VL was ligated into the cloning vector pCR-Blunt. After cut off from pCR-Blunt using enzyme digestion, HGFR-scFv gene was subcloned into the lentiviral transfer vector pRRL-CMV, which was identified by the restriction enzyme digestion and sequencing. The lentiviral expression vector pRRL HGFR-scFv was then tansfected together with the packaging plasmids into HEK293T cells to obtain virus particles, and green fluorescent protein (GFP) expression was detected under a fluorescent microscope. Then the virus particles were used to infect HEK293 cells. The scFv expression was detected by RT-PCR and its biological affinity as antibody was measured by ELISA. RESULTS: The lentiviral expression vector pRRL HGFR-scFv was constructed correctly. After HEK293T cells were transfected with the pRRL HGFR-scFv plasmid, the GFP was visible. After HEK293 cells were infected with virus particles, the scFv antibody expressed could bind to HGFR specifically. CONCLUSION: The lentiviral expression vector of HGFR-scFv was constructed successfully, which would help to study the important role of HGFR in following experiments.

Risk factors for postoperative hypoxemia in patients undergoing Stanford A aortic dissection surgery.

BACKGROUND: The purpose of this study is to identify the risk factors for postoperative hypoxemia in patients with Stanford A aortic dissection surgery and their relation to clinical outcomes. METHODS: Clinical records of 186 patients with postoperative hypoxemia in Stanford A aortic dissection were analyzed retrospectively. The patients were divided into two groups by postoperative oxygen fraction (PaO2/FiO2):hypoxemia group (N=92) and non-hypoxemia group (N=94). RESULTS: We found that the incidence of postoperative hypoxemia was 49.5%. Statistical analysis by t-test and χ2 indicated that acute onset of the aortic dissection (p=0.000), preoperative oxygen fraction (PaO2/FiO2) ≤200 mmHg(p=0.000), body mass index (p=0.008), circulatory arrest (CA) time (p=0.000) and transfusion more than 3000 ml(p=0.000) were significantly associated with postoperative hypoxemia. Multiple logistic regression analysis showed that preoperative hypoxemia, CA time and transfusion more than 3000 ml were independently associated with postoperative hypoxemia in Stanford A aortic dissection. CONCLUSION: Our results suggest that postoperative hypoxemia is a common complication in patients treated by Stanford A aortic dissection surgery. Preoperative oxygen fraction lower than 200 mmHg, longer CA time and transfusion more than 3000 ml are predictors of postoperative hypoxemia in Stanford A aortic dissection.