“小白板”激活小班课堂

在介绍＂小白板＂的应用背景前提下,比较出其特色,介绍其展示形式,阐释其等记录、展示、启智功能意义,为在小班化教育理念下激活课堂探获新路。

Significance of endothelial dysfunction in the pathogenesis of early and delayed radiation enteropathy

This review summarizes the current state of knowledge regarding the role of endothelial dysfunction in the pathogenesis of early and delayed intestinal radiation toxicity and discusses various endothelial-oriented interventions aimed at reducing the risk of radiation enteropathy. Studies published in the biomedical literature during the past four decades and cited in PubMed, as well as clinical and laboratory data from our own research program are reviewed. The risk of injury to normal tissues limits the cancer cure rates that can be achieved with radiation therapy. During treatment of abdominal and pelvic tumors, the intestine is frequently a major close-limiting factor. Microvascular injury is a prominent feature of both early （inflammatory）, as well as delayed （fibroproliferative） radiation injuries in the intestine and in many other normal tissues. Evidence from our and other laboratories suggests that endothelial dysfunction, notably a deficiency of endothelial thrombomodulin, plays a key role in the pathogenesis of these radiation responses. Deficient levels of thrombomodulin cause loss of vascular thromboresistance, excessive activation of cellular thrombin receptors by thrombin, and insufficient activation of protein C, a plasma protein with anticoagulant, anti-inflammatory, and cytoprotective properties. These changes are presumed to be critically involved in many aspects of early intestinal radiation toxicity and may sustain the fibroproliferative processes that lead to delayed intestinal dysfunction, fibrosis, and clinical complications. In conclusion, injury of vascular endothelium is important in the pathogenesis of the intestinal radiation response. Endothelial-oriented interventions are appealing strategies to prevent or treat normal tissue toxicity associated with radiation treatment of cancer.

Relationship between ADP-induced platelet-fibrin clot strength and anti-platelet responsiveness in ticagrelor treated ACS patients

Background Ticagrelor provides enhanced antiplatelet efficacy but increased risk of bleeding and dyspnea. This study aimed to display the relationship between ADP-induced platelet-fibrin clot strength （MAADP） and clinical outcomes in acute coronary syndrome （ACS） patients treated by ticagrelor. Methods Consecutive Chinese-Han patients with ACS who received maintenance dose ofticagrelor on top of aspirin were recruited. After 5-day ticagrelor maintenance treatment, MAADP measured by thrombelastography （TEG） were recorded for the evaluation of ticagrelor anti-platelet reactivity. Pre-specified cutoffs of MAADP 〉 47 mm for high on-treatment platelet reactivity （HTPR） and MAADP 〈 31 mm for low on-treatment platelet reactivity （LTPR） were applied for evaluation. The occurrences of primary ischemic cardiovascular events （including a composite of cardiac death, non-fatal myocardial infarction and stroke）, the Thrombolysis in Myocardial Infarction （TIMI） defined bleeding events, and ticagrelor related dyspnea were recorded after a follow-up of three months. Results Overall, 176 ACS patients （Male： 79.55%, Age： 59.91 ±10.54 years） under ticagrelor maintenance treatment were recruited. The value of MAADP ranged from 4.80% to 72.90% （21.27% ± 12.07% on average）, with the distribution higher skewed towards the lower values. Using the pre-specific cutoffs for HTPR and LTPR, seven patients （3.98%） were identified as HTPR and 144 patients （81.82%） as LTPR. After a follow-up of three months in 172 patients, major cardiovascular events occurred in no patient, but TIMI bleeding events in 81 （47.09%） with major bleedings in three patients. All patients with major bleedings were classified as LTPR. Ticagrelor related dyspnea occurred in 31 （18.02%） patients, with 30 （21.28%） classified as LTPR and no one as HTPR （P = 0.02）. Conclusions In ticagrelor treated ACS patients, MAADP measured by TEG might be valuable for the prediction of major bleeding and ticagrelor related dyspnea. Due to the small number of patients with HTPR after ticagrelor maintenance treatment, larger scale study should be warranted to verify the relationship between MAADP defined HTPR and ticagrelor related ischemic events.

Higher platelet P-selectin in male patients with inflammatory bowel disease compared to healthy males

AIM： To observe if the total amount of platelet P-selectin （tP-selectin） in patients with inflammatory bowel disease （IBD） was related to disease entity or activity, 5-aminosalicylic acid （5-ASA） medication or gender. METHODS： tP-selectin was measured by immunoassay in seventeen IBD patients and twelve healthy controls. RESULTS： Compared to controls, there was no difference of tP-selectin in patients related to disease entity or activity and 5-ASA medication. When the groups were split according to gender the male patient group showed higher levels of tP-selectin compared to male controls （153 ng/mL vs 94 ng/mL, P〈 0.05）. CONCLUSION： Increased tP-selectin levels may alter the inflammatory response and susceptibility to thromboembolic disease. As previously shown with soluble P-selectin, tP-selectin shows gender dependent differences important to consider in future studies.

Total embolization of the main splenic artery as a supplemental treatment modality for hypersplenism

AIM:To study the safety and feasibility of total embolization of the main splenic artery as a supplemental treatment modality for hypersplenism with thrombocytopenia or leukocytopenia accompanying liver cirrhosis.METHODS:Fifteen consecutive patients with hypersplenism due to cirrhosis were enrolled in this study from January 2006 to June 2010.All patients underwent total embolization of the main splenic artery.Clinical symptoms,white blood cell(WBC) and platelet(PLT) counts,splenic volume,and complications of the patients were recorded.The patients were followed up for 1 and 6 mo,and 1,2,3 years,respectively,after operation.RESULTS:Total embolization of the main splenic artery was technically successful in all patients.Minor complications occurred in 13 patients after the procedure,but no major complications were found.The WBC andPLT counts were significantly higher and the residual splenic volume was significantly lower 1 and 6 mo,and 1,2,3 years after the procedure than before the procedure(P < 0.01).Moreover,the residual splenic volume increased very slowly with the time after embolization.All patients were alive during the follow-up period.CONCLUSION:Total embolization of the main splenic artery is a safe and feasible procedure and may serve as a supplemental treatment modality for hypersplenism with thrombocytopenia or leukocytopenia accompanying liver cirrhosis.

Can mean platelet volume play a role in evaluating the severity of acute pancreatitis?

AIM To investigate serum mean platelet volume(MPV) levels in acute pancreatitis(AP) patients and assess whether MPV effectively predicts the disease severity of AP.METHODS We included 117 consecutive patients with AP as the AP group and 34 consecutive patients with colorectal polyps(before endoscopic treatment) as the control group. Complete blood counts, liver function, platelet indices(MPV), coagulation parameters, lactate dehydrogenase(LDH) and C-reactive protein(CRP) were measured on days 1, 2, 3 and 7 after admission. Receiver operating characteristic curves were used to compare the sensitivity and specificity of MPV, white blood cell(WBC), LDH and CRP in predicting AP severity. The Modified Glasgow Prognostic Score(m GPS) and the 2012 revised Atlanta criteria were used to evaluate disease severity in AP.RESULTS MPV levels were significantly lower in the AP group than in the control group on day 1(P = 0.000), day 2(P = 0.029) and day 3(P = 0.001) after admission.In addition, MPV values were lower on day 1 after admission than on day 2(P = 0.012), day 3(P = 0.000) and day 7(P = 0.002) in all AP patients. Based on the m GPS, 78 patients(66.7%) were diagnosed with mild and 39 patients(33.3%) with severe AP. There was no significant difference in mean MPV levels between patients diagnosed with mild and severe AP based on the m GPS(P = 0.424). According to the 2012 revised Atlanta criteria, there were 98 patients(83.8%) without persistent organ failure(OF) [non-severe acute pancreatitis(non-SAP) group] and 19 patients(16.2%) with persistent OF(SAP group). MPV levels were significantly lower in the SAP group than in the non-SAP group on day 1 after admission(P = 0.002). On day 1 after admission using a cut-off value of 6.65 f L, the overall accuracy of MPV for predicting SAP according to the 2012 revised Atlanta criteria(AUC = 0.716) had a sensitivity of 91.8% and a specificity of 47.4% and was superior to the accuracy of the traditional markers WBC(AUC = 0.700) and LDH(AUC = 0.697).CONCLUSION MPV can be used at no additional cost as a useful, noninvasive biomarker that distinguishes AP with persistent OF from AP without persistent OF on day 1 of hospital admission.

Combination therapy reduces the percutaneous coronary intervention acute myocardial infarction incidence of no-reflow after primary in patients with ST-segment elevation

Background No-reflow is associated with an adverse outcome and higher mortality in patients with ST-segment elevation acute myocardial infarction （STEMI） who undergo percutaneous coronary intervention （PCI） and is considered a dynamic process characterized by multiple pathogenetic components. The aim of this study was to investigate the effectiveness of a combination therapy for the prevention of no-reflow in patient with acute myocardial infarction （AMI） undergoing primary PCI. Methods A total of 621 patients with STEMI who underwent emergency primary PCI were enrolled in this study. Patients with high risk of no-reflow （no-flow score 〉 10, by using a no-flow risk prediction model, n = 216） were randomly divided into a controlled group （n = 108） and a combination therapy group （n = 108）. Patients in the controlled group received conventional treatment, while patients in combination therapy group received high-dose （80 mg） atorvastatin pre-treatment, intracoronary administration of adenosine （140 ~tg/min per kilogram） during PCI procedure, platelet membrane glycoprotein lib/Ilia receptor antagonist （tirofiban, 101.tg/kg bolus followed by 0.15 ~tg/kg per minute） and thrombus aspiration. Myocardial contrast echocardiography was performed to assess the myocardial perfusion 72 h after PCI. Major adverse cardiac events （MACE） were followed up for six months. Results Incidence of no-reflow in combination therapy group was 2.8%, which was similar to that in low risk group 2.7% and was significantly lower than that in control group （35.2%, P 〈 0.01）. The myocardial perfusion （A= 13） values were higher in combination therapy group than that in control group 72 h after PCI. After 6 months, there were six （6.3%） MACE events （one death, two non-fatal MIs and three revasculafizations） in combination therapy group and 12 （13.2%） （four deaths, three non-fatal MIs and five revascularizations, P 〈 0.05） in control group. Conclusions Combination of thrombus aspiration, high-dose statin pre-treatment, intmcoronary administration of adenosine during PCI procedure and platelet membrane glycoprotein Ⅱ b/Ⅲa receptor antagonist reduces the incidence of no-reflow after primary PCI in patients with acute myocardial infarction who are at high risk of no-reflow.

Thrombotic microangiopathy-like disorder after living-donor liver transplantation:A single-center experience in Japan

AIM:To investigate thrombotic microangiopathy (TMA)in liver transplantion,because TMA is an infrequent but life-threatening complication in the transplantation field. METHODS:A total of 206 patients who underwent living-donor liver transplantation (LDLT) were evaluated,and the TMA-like disorder (TMALD) occurred in seven recipients. RESULTS:These TMALD recipients showed poor outcomes in comparison with other 199 recipients. Although two TMALD recipients successfully recovered,the other five recipients finally died despite intensive treatments including repeated plasma exchange (PE) and re-transplantation. Histopathological analysis of liver biopsies after LDLT revealed obvious differences according to the outcomes. Qualitative analysis of antibodies against a disintegrin-like domain and metalloproteinase with thrombospondin type 1 motifs (ADAMTS-13) were negative in all patients. The fragmentation of red cells,the microhemorrhagic macules and the platelet counts were early markers for the suspicion of TMALD after LDLT. Although the absolute values of von Willebrand factor (vWF) and ADAMTS-13 did not necessarily reflect TMALD,the vWF/ADAMTS-13 ratio had a clear diagnostic value in all cases. The establishment of adequate treatments for TMALD,such as PE for ADAMTS-13 replenishment or treatments against inhibitory antibodies,must be decided according to each case. CONCLUSION:The optimal induction of adequate therapies based on early recognition of TMALD by the reliable markers may confer a large advantage for TMALD after LDLT.

Association of primary biliary cirrhosis with idiopathic thrombocytopenic purpura

Although both primary biliary cirrhosis (PBC) and idiopathic thrombocytopenic purpura (ITP) are autoimmune diseases, the association of the 2 diseases is rare. Here, we report a case of ITP that developed during the follow-up of PBC in a 74-year- old man. The patient had been diagnosed with PBC 12 years previously, and had received treatment with ursodeoxycholic acid. The platelet count decreased from approximately 60 × 109/L to 8 × 109/L, and the association of decompensated liver cirrhosis (PBC) with ITP was diagnosed. Steroid and immune gamma globulin therapy were successful in increasing the platelet count. Interestingly, human leukocyte antigen genotyping detected the alleles DQB10601 and DRB10803, which are related to both PBC and ITP in Japanese patients. This case suggests common immunogenetic factors might be involved in the development of PBC and ITP.

EFFECT OF 764－3 ON AGGREGATION AND CALCIUM MOVEMENTS IN AEQUORIN－LOADED HUMAN PLATELETS

Washed human platelets were loaded with the Ca2+-sensitive photoprotein, aequorin. using hypoosmotic shock treatment-technique. Then aggregation and cytoplasmic ionized calcium concentration ( [Ca2+] i) changes in response to collagen or thrombin were measured simultaneously in the aequorin-loaded human platelets with a Platelet Ionized Calcium Aggregometer. 764-3. an active component isolated from the Chinese medicinal herb Salvia Miltiorrhiza Bge, inhibited platelet [Ca2+]i rise as well as aggregation evoked by collagen or thrombin in the presence of extracellular Ca2+. After the extracellular Ca2+. was removed by addition of EGTA, collagen or thrombin. causing no aggregation. still elicited platelet [Ca2+] i rise which reflected Ca2+ mobilization from intraplatelet stores. Under this condition, 764-3 could also suppress platelet [Ca2+] i rise. Analysis shows that 764-3 inhibrts platelet Ca2+ influx and Ca2+ mobilization with similar potency. which accounts for its suppression of platelet [Ca2+] i rise, and must contribute to its inhibition of platelet aggregation.

Comparing irinotecan/cisplatin with etoposide/cisplatin in patients with ED-SCLC: A meta-analysis of efficacy and toxicity

Objective： Irinotecan in combination with cisplatin for extensive-stage disease small-ceU lung cancer （ED-SCLC） patients has gained wide interest. Varying results for this treatment underpin the need for a synthesis of evidence. Methods： We conducted a literature-based meta-analysis to quantify the magnitude of the benefit comparing irinotecan in combination with cisplatin （IP） with etoposide in combination with cisplatin （EP） in ED-SCLC patients. The primary outcome was overall survival （OS） and progression-free survival （PFS）; secondary outcomes included overall response rate, 1- and 2-year survival rates, disease control rate and toxicity. Results： Four trials including 1,541 patients were identified in the analysis. No positive results （P〈0.05） were seen： OS （HR=0.85, CI95%=0.71-1.01; P=-0.08） with high heterogeneity （Chi2=7.76, dr=-3 [P=-0.05]; I2=61%）, PFS （HR=0.91, CI95%=0.74-1.28; P=-0.36） with high heterogeneity （Chi2=11.96, df=3 [P=-0.008]; I2=75%）, overall response rate（OR=1.16; CI95%=0.79-1.70; P=0.45）, disease control rate （OR=1.01; CI95%=0.74-1.38; P=0.95）, 1-year survival rate （OR = 1.30; CI95%=0.98-1.72; P=0.07） and 2-year survival rate （OR=1.97; CI95%=0.95-4.09; P=-0.07）. Fewer patients who received IP suffered severe hematologic toxicities （grade≥3）, such as neutropenia, thrombocytopenia and leucopenia. However, severe non-hematologic toxicities （grade≥3）, such as diarrhea, nausea, vomiting, fatigue, anorexia, and dehydration, were more common among patients who received IP. Conclusion： IP does not lengthen the overall survival or progression-free survival compared with EP in patients with ED-SCLC Fewer patients receiving IP had grade ≥ 3 hematological toxicities of nentropenia, leucopenia and thrombocytopenia, but more had grade≥3 diarrhea, nausea, vomiting, fatigue, anorexia and dehydration.

ANTI-HUMAN PLATELET TETRASPANIN(CD9)MONOCLONAL ANTIBODIES INDUCE PLATELET INTEGRIN αbβ3 ACTIVATION IN A Fc RECEPTOR INDEPENDENT FASHION

This study characterized the activation of platelet integrin α bβ3 induced by two anti human platelet tetraspanin monoclonal antibodies(mAbs),HI117 and SJ9A4. Methods.Using 125 I labeled human fibrinogen(Fg),specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured as indication of activation of platelet integrin αbβ3 by the two mAbs. Results.HI117 and SJ9A4(10μg/ml and 20μg/ml) induced evident specific Fg binding to human platelets,suggesting that the two mAbs evoked activation of platelet integrin αbβ3.Further study indicated that HI117 and SJ9A4 induced integrin αⅡbβ3 activation independent of platelet Fc receptors, and that HI117 and SJ9A4 induced integrin αbβ3 activation was inhibited by sphingosing, aspirin, apyrase, and/or PGI2. Conclusion.The anti platelet tetraspanin(CD9)mAbs,HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 activation independent of Fc receptors.Three signaling pathways,i.e.thromboxane,secreted ADP, and cAMP pathways may be involved in the process,with protein kinase C activation presumably being the common step of the three pathways.

LIPOPOLYSACCHARIDE INDUCES EXPOSURE OF FIBRINOGEN RECEPTORS ON HUMAN PLATELETS

The effect of lipopolysaccharide (LPS) on the exposure of platelet fibrinogen receptors was investigated. The results showed that:l)LPS increased the binding of fibrinogen-gold complexes to platelets and the labels were primarily limited to shape-changed platelets; 2) LPS caused a dose-dependent rise in intracellular Ca2+ concentration in platelets; 3)LPS induced the activation of platelet protein kinase C (PKC) and the phosphorylation of glycoprotein llla (GPllla) which was inhibited by H-7. All these results suggest that stimulation of platelets with LPS causes a conformational change in glycoprotein llb/llla (GPllb/llla)through platelet shape change and /or phosphorylation of GPllla via PKC, which serves to expose the fibrinogen binding sites of GPllb/llla on human platelets.

Esophageal combined carcinomas:Immunohoistochemical and molecular genetic studies

Primary esophageal combined carcinoma is very rare. The authors herein report 2 cases. Case 1 was a com- bined squamous cell carcinoma and small cell carci- noma, and case 2 was a combined squamous cell carci- noma, adenocarcinoma, and small cell carcinoma. Case 1 was a 67-year-old man with complaints of dysphagia. Endoscopic examination revealed an ulcerated tumor in the middle esophagus, and 6 biopsies were obtained. All 6 biopsies revealed a mixture of squamous cell car- cinoma and small cell carcinoma. Both elements were positive for cytokeratin, epithelial membrane antigen, and p53 protein, and had high Ki-67 labeling. The small cell carcinoma element was positive for synaptophysin, CD56, KIT, and platelet-derived growth factor-~ （PDG- FRA）, while the squamous cell carcinoma element was not. Genetically, no mutations of K/Tand PDGFRA were recognized. The patient died of systemic carcinomato- sis 15 mo after presentation. Case 2 was a 74-year-old man presenting with dysplasia. Endoscopy revealed a polypoid tumor in the distal esophagus. Seven biopsies were taken, and 6 showed a mixture of squamous cell carcinoma, small cell carcinoma, and adenocarcinoma. The 3 elements were positive for cytokeratins, epithe-lial membrane antigen, and p53 protein, and had high Ki-67 labeling. The adenocarcinoma element was posi- tive for mucins. The small cell carcinoma element was positive for CD56, synaptophysin, KIT, and PDGFRA, but the other elements were not. Mutations of KIT and PDGFRA were not recognized. The patient died of sys- temic carcinomatosis 7 mo after presentation. These combined carcinomas may arise from enterochromaf- fin cells or totipotential stem cell in the esophagus or transdifferentiation of one element to another. A review of the literature was performed.

Effect of resveratrol on platelet aggregation in vivo and in vitro

OBJECTIVE: Low or moderate consumption of red wine has a greater benefit than the consumption of other beverages in the prevention of atherosclerosis and coronary heart disease and this is increasingly attributed to the polyphenol compounds in red wine, such as resveratrol. In the present study, we investigated the effect of resveratrol on platelet aggregation in vitro and in vivo. METHODS: Platelet aggregation in rabbits and normal subjects was measured using Born's method. RESULTS: Resveratrol, at 10 - 1000 micromol/L, significantly inhibited platelet aggregation in vitro induced by collagen, thrombin, and ADP in healthy subjects. The inhibitory effect was concentration-dependent. Hypercholesterolemia induced by high-cholesterol diet enhanced ADP-induced platelet aggregation. Resveratrol 4 mg x kg(-1) x d(-1) inhibited ADP-induced platelet aggregation in vivo despite no changes in serum lipid levels. CONCLUSIONS: Resveratrol inhibits platelet aggregation both in vitro and in vivo. This may be one of the mechanisms by which resveratrol prevents atherosclerosis.

Hemocompatibility and cytocompatibility of diblock copolymer poly(2-ethyl-2-oxazoline)-poly(D,L-lactide)-based micelles

A synthetic diblock copolymer poly（2-ethyl-2-oxazoline）-poly（D,L-lactide） （PEOz-PLA） can self-assemble into micelles with an increased efficiency of drug delivery. However, the interactions of blood-micelles and cell-micelles remain unclear. In the present study, we aimed to assess the hemocompatibility and cytocompatibility of PEOz-PLA micelles in order to clarify its potentials as carriers for drug delivery. Blood compatibility of the micelles was evaluated by hemolysis analysis, coagulation test, platelet activation investigation and assessment of their interaction with protein. The results revealed that PEOz-PLA micelles had a favorable blood compatibility. In addition, PEOz-PLA micelles showed a good cytocompatibility through SRB assay, presenting only negligible cytotoxicity when incubated with KBv cells. Taken together, PEOz-PLA micelles could be used as a hemocompatible and cytocompatible drug carrier for intravenous administration.

Platelet transfusion refractoriness after T-cell-replete haploidentical transplantation is associated with inferior clinical outcomes

Haploidentical stem cell transplantation (haplo-SCT) has been an alternative source of bone marrow for patients without human leukocyte antigen (HLA)-matched donors. The aim of this study was to investigate the relationships between platelet transfusion refractoriness (PTR) and clinical outcomes in the setting of haplo-SCT. Between May 2012 and March 2014, 345 patients who underwent unmanipulated haplo-SCT were retrospectively enrolled. PTR occurred in 20.6% of all patients. Patients in the PTR group experienced higher transplant-related mortality (TRM, 43.7% vs. 13.5%, P<0.001), lower overall survival (OS, 47.9%vs. 76.3%, P<0.001) and lower leukemia-free survival (LFS, 47.9% vs. 72.3%, P<0.001) compared to patients in the non-PTR group. The multivariate analysis showed that PTR was associated with TRM (P=0.002), LFS (P<0.001), and OS (P<0.001).The cumulative incidences of PTR in patients receiving >12 platelet (PLT) transfusions (third quartile of PLT transfusions) were higher than in patients receiving either >6 (second quartile) or >3 (first quartile) PLT transfusions (56.1% vs. 41.6% vs. 28.2%,respectively; P<0.001). The multivariate analysis also showed that PTR was associated with the number of PLT transfusions(P<0.001). PTR could predict poor transplant outcomes in patients who underwent haploidentical SCT.

Relationship between trauma-induced coagulopathy and progressive hemorrhagic injury in patients with traumatic brain injury

Progressive hemorrhagic injury （PHI） can be divided into coagulopathy-related PHI and normal coagu- lation PHI. Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy （TIC）. Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality. In this review, we discussed some mechanisms in TIC, which is of great importance in the development of PHI, including tissue factor （TF） hypothesis, protein C pathway and thrombocytopenia. The main mechanism in the relation of TIC to PHI is hypocoagulability. We also reviewed some coagulopathy parameters and proposed some possible risk factors, predictors and therapies.

Platelet-mediated adhesion facilitates leukocyte sequestration in hypoxia-reoxygenated microvessels

Leukocyte transendothelial migration and sequestration are two distinct outcomes following leukocyte adhesion to endotheli- um during ischemia-reperfusion injury, in which platelets may play a pivotal role. In the present study, we established an in vitro hypoxia-reoxygenation model to mimic ischemia-reperfusion injury and found platelet pre-incubation significantly in- creased leukocyte adhesion to endothelial cells after hyoxia-reoxygenation （over 67%）. Blockade of endothelial-cell-expressed adhesion molecules inhibited leukocyte direct adhesion to endothelial cells, while platelet-mediated leukocyte adhesion was suppressed by blockade of platelet-expressed adhesion molecules. Further experiments revealed platelets acted as a bridge to mediate leukocyte adhesion, and platelet-mediated adhesion was the predominant pattern in the presence of platelets. However, platelet pre-incubation significantly suppressed leukocyte transendothelial migration after hypoxia-reoxygenation （over 31%）, which could be aggravated by blockade of endothelial-cell-expressed adhesion molecules, but alleviated by blockade of plate- let-expressed adhesion molecules. This would indicate that platelet-mediated adhesion disrupted leukocyte transendothelial migration. An in vivo meseuteric ischemia-reperfusion model demonstrated leukocyte transfusion alone caused mild leukocyte adhesion to reperfused vessels and subsequent leukocyte infiltration, while simultaneous leukocyte and platelet transfusion led to massive leukocyte adhesion and sequestration within reperfused microvessels. Our studies revealed platelets enhanced leu- kocyte adhesion to endothelial cells, but suppressed leukocyte transendothelial migration. Overall, this leads to leukocyte se- questration in hypoxia-reoxygenated microvessels.

Improved biocompatibility of phosphorylcholine end-capped poly(butylene succinate)

In this work, the biocompatibility of a biomimetic, fully biodegradable ionomer phosphorylcholine (PC)-functionalized poly(butylene succinate) (PBS-PC) was investigated by means of hemolysis, platelet adhesion, protein adsorption and cytotox- icity experiments. The reference materials were poly(butylene succinate) (PBS) and chloroethylphosphoryl functionalized poly(butylene succinate) (PBS-Cl). The hemolysis rates (HR) of the leaching solutions of PBS, PBS-Cl and PBS-PC were all lower than the safe value, and the rate of PBS-PC was reduced to 1.07%. Scanning electron microscopy (SEM) measurements showed that platelet adhesion and aggregation were significant on both PBS and PBS-Cl surface. In contrast, very few platelets were observed on PBS-PC surface. Bicinchoninic acid (BCA) measurements revealed that the adsorption amounts of bovine serum albumin (BSA) and bovine plasma fibrinogen (BPF) on PBS-PC surface were 52% and 72% reduction respectively compared with those on PBS surface. Moreover, non-cytotoxicity of both PBS-PC particles and its leaching solution was sug- gested by MTT assay using mouse L929 fibroblast cells. All the results demonstrated that the biocompatibility of PBS could be greatly improved by PC end-capping strategy. This PC functionalized polyester may have potential applications in biological environments as a novel carrier for controlled drug release and scaffold for tissue engineering.