Objective To investigate the changes in intrapulmonary shunting during controlled hypotension induced by sodium nitroprusside(SNP)in patients undergoing naso-endoscopic operation.Methods Forty ASAⅠorⅡpatients of both sexes(23 male,17 female)aged 16-50 yrs weighing 50-75 kg undergoing naso-endoscopic operation under general anesthesia with muscle relaxation and mechanical ventilation were studied.Radial artery was cannulated for direct BP monitoring and blood sampling.Right internal jugular vein was cannulated and the catheter was advanced into right ventricle.Blood sample taken from right ventricle was used as mixed venous blood instead of blood from pulmonary artery.ECG,MAP,HR and P_(ET) CO_2 were continuously monitored during operation Cardiac output was monitored with noninvasive cardiac function monitor(NC-COM.)based on impedance principle.SNP infusion was started at the beginning of operation at 1-3?g?kg~(-1)?min~(-1) and was then adjusted.MAP was reduced by 30%-40% and maintained at this level until the end of operation.Blood samples were taken from artery and right ventricle simultaneously before SNP infusion(T_1,baseline)at 30 and 60 min of hypotension(T_2,T_3)and at 20 min after BP returned to the baseline level(T_4)for blood gas analysis.Qs/Qt was calculated.Results Qs/Qt was significantly increased during controlled hypotension at T_2 and T_3 as compared to the baseline value(P＜0.01)and returned to the baseline level at T_4.HR was increased and cardiac output and stroke volume was significantly reduced during hypotension as compared to the baseline value.Conclusion The intrapulmonary shunting is increased and the hemodynamics is depressed during SNP-induced controlled hypotension and they return rapidly to baseline level after SNP is discontinued.No hypoxemia develops during SNP- induced hypotension.

BACKGROUND:The biological substances fixed onto the implant surface, including specific proteins, enzymes, polypeptides, could promote the proliferation and differentiation of osteogenic cells in order to achieve a good osteogenic effect.
OBJECTIVE:To introduce the biological characteristics of the arginine-glycine-aspartic acid (RGD) peptides, cellbiological behavior and implant osseointegration in osteoporosis.
METHODS:Authors retrieved the relevant articles in PubMed database (January 1984 to January 2013), Wanfang database (January 2002 to December 2012) and CHKD database (January 2002 to December 2012) using the key words“RGD peptides, osteoporosis, bone marrow mesenchymal stem cells, osseointegration, osteoblast, induced differentiation”. Papers were included concerning the biological characteristics of RGD peptides, the biological behavior of cells and the bone-implant integration in osteoporosis.
RESULTS AND CONCLUSION:Osseointegration on the surface between implant and bone tissue can be further improved by grafting biological y active substance. Bionics modification, to simulate the extracellular matrix environment in vivo, can promote celladhesion and growth, which is an effective way to improve osseointegration and is also an important direction of research in the field of tissue engineering recently. The future research is focused on designing specific and efficient polypeptides and simple and effective fixation methods.

OBJECTIVE: To analyses the causes and prevention of systemic complications of functional endoscopic sinus surgery (FESS) in patients with chronic rhinosinusitis. METHOD: Three typical cases were reported including their medical history, preoperative diagnosis, medications during preoperational period, complications and treatment. The causes and preventive measures of systemic complications were analyzed. RESULT: Three patients were all suffered from chronic rhinosinusitis with nasal polyps (CRSwNP). After FESS, 1 case was complicated with coma and hyponatremia, 1 case with acute myocardial infarction, and 1 case with lower extremity deep venous thrombosis. The patient with coma and hyponatremia was soon waked after intravenous infusion of 10% sodium chloride. Two patients with acute myocardial infarction and lower extremity deep venous thrombosis were soon completely rehabilitated after emergency thrombolytic therapy and endovascular intervention. Three patients were completed recovered from their systemic complications without any severe sequela. CONCLUSION Systemic hemostatic drugs should be banned in patients with hypercoagulable state in perioperation period of FESS in order to avoid severe systemic complications. Timely vascular interventional treatment can prevent severe sequels.
Cardiovascular Diseases ; Chronic Disease ; Endoscopy ; Humans ; Myocardial Infarction ; Nasal Polyps ; Postoperative Complications ; Rhinitis ; surgery ; Sinusitis ; Venous Thrombosis

BACKGROUND:The linkage and synergistic effect of adaptor proteins can effectively regulate signal transduction of T cel s, which can form a limit or amplification cascade to realize the complex immune function of T cel s. C-terminal Src kinase (Csk)-binding protein (Cbp) is an adaptor protein, which mainly exert the negative feedback regulation of Src kinase activity. This negative feedback effect depends on Y317 of Cbp, which may be involved in the SH2 domain of Csk. OBJECTIVE:To explore the effects of high expression of Cbp on ultrastructure and related biological function of Jurkat cel s. METHODS:The virus particles were constructed with expressing enhanced green fluorescent protein (EGFP) only and Cbp-EGFP fusion protein to transfect Jurkat cel s. There were untransfected group (Jurkat group), negative control group (transfected with expression of EGFP virus only), and Cbp group (transfected with Cbp-EGFP virus). RESULTS AND CONCLUSION:Confocal microscope showed that cel transfection efficiency was more than 95%and Cbp was located on the cel membrane. Optical microscope showed after transfection with Cbp-EGFP virus, more Jurkat cel s shrunk, with poor size uniformity. Apoptosis detection showed that after transfection with Cbp-EGFP virus, the number of apoptotic and necrotic cel s was greatly increased. Cbp mRNA expression was increased, Csk expression was decreased obviously and lymphocyte-specific protein tyrosine kinase expression was increased. So, in Jurkat cel s, the high expression of Cbp can decrease the uniformity of cel s and increase the necrosis cel s, thus inhibiting the signal transduction.

Objective To establish the reference value of liver virtual touch tissues quantification (VTQ) values in healthy subjects. Methods Liver stiffness was measured with Siemens Acuson S2000 ultrasound system in totally 300 healthy subjects. The first one hundred healthy subjects received VTQ measurements in four parts (superficial and deep parts of right lobe, superficial and deep parts of left lobe). Then the achievement rate in different part of liver was calculated to choose the suitable measuring position. On the other hand, the reproducibility was analyzed with intraclass correlation coefficient (ICC). The last two hundred healthy subjects received VTQ measurements in the suitable position only. The reference value of VTQ was calculated using (x-)±1.96s. Results It was stable to measure liver stiffness with VTQ technique. The achievement rate was high in right lobe, and the deep parts of right lobe was the best measuring position. There was significant difference of VTQ value between males and females (P＜0.001), while the VTQ value was similar in different age groups. The reference value was 0.79-1.57 m/s in males and 0.74-1.40 m/s in females. Conclusion Liver VTQ value in healthy subjects are different between males and females.

Objective To evaluate the feasibility of virtual touch tissues quantification (VTQ) technique in the assessment of liver fibrosis and to find the suitable measuring position of VTQ. Methods Liver stiffness was measured with Acuson S2000 ultrasound system in totally 533 subjects including healthy people ( n = 302), patients with hepatitis B virus(HBV) ( n = 191) and patients with fatty liver ( n =40). Each subject received VTQ measurements in four parts (superficial and deep parts of right lobe, and superficial and deep parts of left lobe) and every part was measured five times to get five values. The reproducibility of different part of VTQ was analyzed with intraclass correlation coefficient (ICC). Results The achievement rate was high in both right and left lobes,especially in right lobe. The lowest rate was from the deep part of left lobe. Except deep part of left hepatic lobe in fatty liver,all parts of liver in all groups of patients were with ICC higher than 0. 75. In deep part of right lobe, VTQ values were (1.12 ± 0. 19)m/s in control group subjects, (1.83 ± 0. 62)m/s in patients with hepatitis B virus and (1.05 ± 0. 25)m/s in patients with fatty liver. There was significant difference of VTQ value between control group and patients with HBV ( P = 0.000), also between patients with HBV and patients with fatty liver ( P = 0.000). Conclusions It is stable to measure liver stiffness with VTQ technique, which is a new method to evaluate liver stiffness noninvasively. Right hepatic lobe is the most suitable position to be measured.

Objective:To investigate the effects of chitin on atopic dermatitis in an OVA induced AD murine model.Methods:Twenty-eight BALB/c mice were randomly divided into three groups:the normal control group (N)(8),the chitin group(E) (10) and the AD model group(M)(10).The murine model of atopic dermatitis was established through intraperitoneal injection of OVA followed by repeated epicutaneous application of OVA on mice back skin( AD model group).During the set up of AD murine model,mice of the chitin group were given intragastric gavage of 3 mg/d for 4 weeks.At the end of the experiment, the mice were sacrificed and skin lesions were biopsied for histological study.HE and O-toluidine stained paraffin sections were observed under microscope.The spleen cells were cultured and challenged with OVA and chitin,respectively,the supernatant was obtained for cytokine determination.Serum levels of total and OVA-specific IgE and total IgG2a were determined with ELISA.Results:Chitin significantly inhibited skin inflammation induced by OVA.Compared with the AD model group,the thickness of the epidermis and dermis in the chitin group were obviously decreased.The numbers of dermal infiltrated inflammatory cells,eosinophils and mast cells were significantly decreased in the chitin group compared with the AD model group ( P<0.05-0.001 ).The serum level of total IgE and OVA-specific IgE were significantly lower in the chitin group than in the AD model group(P<0.05-0.001),while the serum level of IgG2a in the chitin group was significantly higher than that of the AD model group( P<0.001).The cultured spleen cells of the chitin group produced significantly higher levels of IL-12 and IFN-γ,but lower level of IL-4 compared with those of the AD model group after OVA challenge (P<0.05).Conclusion:Chitin can inhibit the inflammation and decease the seum level of IgE in the murine AD model.The antiallergic effect of chitin might be associated with the induced production of Th1 type cytokines by mice spleen cells.

Animals ; Chlorine Compounds ; toxicity ; Dose-Response Relationship, Drug ; Female ; Lung ; drug effects ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; biosynthesis ; genetics ; Tumor Necrosis Factor-alpha ; biosynthesis ; genetics

Objective To investigate the effects of p300/CBP on histone acetylation of Foxp3 gene and its roles in the immunological pathogenesis of Kawasaki disease (KD).Methods Forty-six children with KD and twenty-eight age-matched health children were consented to participate in this study.Co-immunoprecipitation and real-time PCR were performed to detect Foxp3-associated acetylation levels of histone H4 and binding abilities of p300, CBP, pSmad3 (phosphorylated mothers against decapentaplegic homolog 3) and NF-AT (nuclear factor of activated T cells) with Foxp3 gene in CD4+ T cells.The percentages of CD4+CD25high Foxp3+ cells (Treg) and the expression of Foxp3, CTLA4 (cytotoxic T-lymphocyte-associated protein 4), p300, CBP, TGF-βRⅡ (transforming growth factor β receptor Ⅱ) and pLAT1 at protein level were analyzed by flow cytometry.Quantitative real-time PCR was used to measure the expression of Foxp3, IL-10, TGF-β, TGF-βRⅠ, Egr-1 (early growth response protein 1), RARα (retinoic acid receptor α) and PLCγ1 (phospholipase C-γ1) in Treg cells at mRNA level.Plasma concentrations of TGF-β and retinol acid (RA) were measured by enzyme-linked immunosorbent assay.Results (1) The percentages of Treg cells, levels of Foxp3 and molecules associated with suppressive function of Treg cells (TGF-β, IL-10 and CTLA4), acetylation levels of histone H4 associated with promoter, conserved non-coding DNA sequence 1 (CNS1) and CNS2 of Foxp3 gene decreased remarkably during acute KD (P<0.05), but were restored after IVIG therapy (P<0.05).Meanwhile, all of the aforementioned items in KD patients with coronary artery lesions (KD-CAL+) were lower than those without coronary artery lesions (KD-CAL-) (P<0.05).No significant differences in histone H4 acetylation associated with CNS3 were found among different groups (P>0.05).(2) The levels of p300 and CBP in Treg cells and their binding abilities with Foxp3 gene were down-regulated significantly during acute KD (P<0.05), but were restored to some extent after IVIG treatment (P<0.05).The Foxp3-associated histone acetylation was positively correlated with the expression of p300 and CBP at mRNA level during acute KD (r=0.65, 0.42, P<0.05).Furthermore, the expression of p300 and CBP and their binding abilities with Foxp3 gene in KD-CAL+ group were lower than those in KD-CAL-group (P<0.05).(3) Compared with healthy subjects, plasma concentrations of TGF-β and RA and the expression of TGF-βRⅠ/Ⅱ/Egr-1, RARα and pLAT1/PLCγ1 were down-regulated during acute KD (P<0.05);the binding abilities of pSmad3 and NFAT with Foxp3 gene were reduced remarkably in patients with acute KD (P<0.05).All the items mentioned above were restored after IVIG treatment (P<0.05).Moreover, the ten items aforementioned in KD-CAL+ group were lower than those in KD-CAL-group (P<0.05).(4) Higher acetylation levels of histone H4 associated with promoter, CNS1 and CNS2, and enhanced binding abilities of p300 and CBP with Foxp3 gene were found in CD4+ T cells isolated from patients with acute KD after co-stimulation with TGF-β, RA and anti-CD3/CD28 antibodies as compared with those in CD4+ T cells without stimulation (P<0.05).However, no statistical difference in the acetylation level of histone H4 associated with CNS3 was found between the two groups (P>0.05).Conclusion Hypoacetylation of histone H4 associated with Foxp3 gene caused by insufficient expression of p300/CBP and their impaired binding abilities might be involved with immune dysfunction in KD.IVIG therapy regulates the expression of p300/CBP and their binding abilities with Foxp3 gene through up-regulating TGF-β signal.

Objective To investigate the effects of SMYD3 and MLL5 on histone methylation of Transcription factor forkhead box protein 3 (Foxp3) gene and its roles in the immunological pathogenesis of Kawasaki disease (KD). Methods Forty-two children with KD and 26 age-matched healthy children were consented to participate in this study. Co-Immunoprec-ipitation and real-time polymerase chain reaction (PCR) was performed to determine Foxp3-associated histone methylation levels of H3K4me3 and H3K27me3, and binding levels of SMYD3 and MLL5 with Foxp3 gene in CD4+T cells. The proportion of CD4+CD25high Foxp3+cells (Treg) and protein levels of Foxp3, cytotoxic T lymphocyte associated antigen-4 (CTLA4), TGF-βRⅡand pSmad3 were analyzed by flow cytometry. Quantitative real-time PCR was used to evaluate levels of Foxp3, interleukin (IL)-10, GITR, TGF-βRⅠand RARαmRNA in CD4+T cells. Plasma concentrations of TGF-βand retinol acid (RA) were measured by enzyme-linked Immunosorbent assay. Independent-samples t-test was used as the statistical method in this study. Results ① The proportion of Treg, expression levels of Foxp3 and molecules associated with suppressive function of Treg cells(IL-10, GITR and CTLA4), and histone methylation levels of H3K4me3 associating with promoter, conserved non-coding DNA sequence (CNS) 1 and CNS2 of Foxp3 gene decreased remarkably during acute KD [Promoter:(5.4±1.8)%vs (9.1±2.2)%;CNS1:(2.6±0.9)% vs (3.8±1.1)%; CNS2: (2.4±0.8)% vs (4.2±1.0)%; t=5.50, 6.02, 9.56, 7.92, 7.97, 4.76, 7.73, 5.01, 8.66; P<0.05], and restored after intravenous immunoglobulins (IVIG) therapy [Promoter: (7.2 ±2.1)% vs (5.4 ±1.8)%; CNS1:(3.6±1.4)% vs (2.6±0.9)%; CNS2: (3.6±1.4)% vs (2.4±0.8)%; t=5.56, 4.59, 7.01, 6.04, 5.89, 4.83, 4.45, 4.00, 5.12; P<0.05]. Meanwhile, the nine former items in KD patients with coronary artery lesions (KD-CAL+) were lower than those without coronary artery lesions (KD-CAL-) [Promoter: (4.11±1.45)% vs (6.16±1.93)%; CNS1:(1.99±0.87)%vs (2.96±1.10)%;CNS2: (1.75±0.63)%vs (2.72±1.16)%;t=6.28, 3.24, 4.56, 3.69, 3.38, 4.40, 3.65, 3.00, 3.51; P<0.05]. No significant difference of H3K4me3 associated with CNS3 and H3K27me3 were found among the groups (t=1.03, 0.91, 1.48 and 0.79, 0.82, 1.53; P>0.05). ② Binding levels of SMYD3 and MLL5 with Foxp3 gene in CD4+T cells were down-regulated significantly during acute KD (t=6.63, 6.15; P<0.05), and restored to some extent after IVIG treatment (t=5.36, 4.56; P<0.05). Positive correlations between binding levels of SMYD3 and MLL5 and expression level of Foxp3 mRNA were detected in patients with acute KD (r=0.62、0.45, P<0.05). Furthermore, Binding levels of SMYD3 and MLL5 with Foxp3 gene in KD-CAL+group were lower than those in KD-CAL- group (t=4.11, 4.31; P<0.05). ③ Compared with healthy controls, plasma concentration of TGF-β and RA, and expressions of TGF-βRⅡ, TGF-βRⅠ, pSmad3 and RARα were down-regulated during acute KD (t=11.54, 12.81, 7.43, 16.10, 8.25, 12.06; P<0.05), and elevated remarkably after IVIG treatment (t=8.40, 6.24, 5.94, 11.78, 6.27, 8.30; P<0.05). Simultaneously, all the items aforementioned in KD-CAL+ group were found to be lower than those in KD-CAL-group (t=3.58, 3.30, 3.82, 5.27, 4.71, 3.78; P<0.05). Conclusion Hypomethylation of H3K4me3 associated with Foxp3 gene caused by insufficient binding levels of SMYD3/MLL5 may be involved with immune dysfunction in Kawasaki disease.