Study on Platelet Adhesion and Aggregation Induced by Gradient Shear Stress Using Microfluidic Chip Technology / 中国实验血液学杂志

OBJECTIVE@#To study the effect of gradient shear stress on platelet aggregation by microfluidic chip Technology.@*METHODS@#Microfluidic chip was used to simulate 80% fixed stenotic microchannel, and the hydrodynamic behavior of the stenotic microchannel model was analyzed by the finite element analysis module of sollidwork software. Microfluidic chip was used to analyze the adhesion and aggregation behavior of platelets in patients with different diseases, and flow cytometry was used to detect expression of the platelet activation marker CD62p. Aspirin, Tirofiban and protocatechuic acid were used to treat the blood, and the adhesion and aggregation of platelets were observed by fluorescence microscope.@*RESULTS@#The gradient fluid shear rate produced by the stenosis model of microfluidic chip could induce platelet aggregation, and the degree of platelet adhesion and aggregation increased with the increase of shear rate within a certain range of shear rate. The effect of platelet aggregation in patients with arterial thrombotic diseases were significantly higher than normal group (P<0.05), and the effect of platelet aggregation in patients with myelodysplastic disease was lower than normal group (P<0.05).@*CONCLUSION@#The microfluidic chip analysis technology can accurately analyze and evaluate the platelet adhesion and aggregation effects of various thrombotic diseases unde the environment of the shear rate, and is helpful for auxiliary diagnosis of clinical thrombotic diseases.

Main Factors Influencing the Platelet Spreading / 中国实验血液学杂志

OBJECTIVE@#To explore the main factors of platelet spreading and provide the foundation for related research.@*METHODS@#Platelets (2×107/ml) were draw from C57BL/6J mouse and kept at 22 ℃ for 1-2 hours. Platelets (2×107/ml) were were allowed to adhere and spread on the fibrinogen-coated slides, after staining F-actin in platelets, the platelets were observed with the confocal microscopy. The effects of different concentrations of fibrinogen (10 μg/ml, 30 μg/ml, 100 μg/ml) and kinds of agonists ［thrombin(0.01,0.05,0.1 U/ml), ADP（5,10,20 μmol/L）, U46619（0.125,0.25,0.5 μmol/L）］ on platelets were analyzed. The platelet spreading was successful if the spreading rate was higher after treated with agonists.@*RESULTS@#Compared to the group which coated with 10 μg/ml and 100 μg/ml fibrinogen, the platelet density is optimal when coated with 30 μg/ml fibrinogen. In addition, under the stimulation of thrombin, ADP and U46619, the spreading rate of platelets showed a certain concentration-dependent increasing.@*CONCLUSION@#The platelet spreading is easily influenced by various factors, the platelet spreading can be induced successfully at 0.1 U/ml thrombin, 20 μmol/L ADP and 0.5 μmol/L U46619 on the slide coated with 30 μg/ml fibrinogen.

Effects of material interfaces on orientation and function of fibrinogen / 生物医学工程学杂志

Fibrinogen (Fg) in human plasma plays an important role in hemostasis, vascular repair and tissue integrity. The surface chemistry of extracellular matrix or biological materials affects the orientation and distribution of Fg, and changes the exposure of integrin binding sites, thereby affecting its adhesion function to platelets. Here, the quantity, morphology and side chain exposure of Fg adsorbed on hydrophilic, hydrophobic and avidin surfaces were measured by atomic force microscopy (AFM) and flow cytometry (FCM), then the rolling behavior of platelets on Fg was observed through a parallel plate flow chamber system. Our results show that the hydrophobic surface leads to a large amount of cross-linking and aggregation of Fg, while the hydrophilic surface reduces the adsorption and accumulation of Fg while causing the exposure and spreading of the α chain on Fg and further mediating the adhesion of platelets. Fg immobilized by avidin / biotin on hydrophilic surface can maintain the monomer state, avoid over exposure and stretching of α chain, and bind to the platelets activated by the A1 domain of von Willebrand factor instead of inactivated platelets. This study would be helpful for improving the blood compatibility of implant biomaterials and reasonable experimental design of coagulation

Perfil demográfico y epidemiológico de pacientes con Hemofilia y von Willebrand atendidos en el Área de Estomatología del Hospital de Especialidades Carlos Andrade Marín / Demographic and epidemiological profile of patients with Hemophilia and von Willebrand treated in the Stomatology Area of the Carlos Andrade Marín Specialties Hospital

INTRODUCCIÓN. Las alteraciones hereditarias de la hemostasia son patologías raras, dentro de estas se encuentran: Hemofilia A, Hemofilia B y von Willebrand. La hemofilia es un trastorno hereditario, ligado al cromosoma X, causado por ausencia o actividad reducida del factor VIII o IX. La enfermedad de von Willebrand es causada por la deficiencia del factor VIII. OBJETIVO. Determinar el perfil demográfico y epidemiológico de pacientes con Hemofilia y von Willebrand. MATERIALES Y MÉTODOS. Estudio observacional, descriptivo, transversal. La población de estudio fueron 133719 con una muestra de 144 pacientes, los criterios de inclusión fueron: pacientes de ambos sexos entre 2 a 88 años de edad, con diagnóstico de Hemofilia A, B, von Willebrand. Atendidos en la consulta externa del Área de Estomatología del Hospital de Especialidades Carlos Andrade Marín, en el periodo 2015-2018. Datos obtenidos del sistema AS400, analizados en el programa International Business Machines Statistical Package for the Social Sciences, Versión 22.0. RESULTADOS. El 77,0% (111; 144) perteneció al género masculino. El rango de edad fue entre 23 y 33 años con 24,0% (34; 144). Tuvieron Hemofilia A 62,0% (93; 144); Hemofilia B 6,0% (9; 144); von Willerbrand 28,0% (42; 144). El 50,0% (77; 144) recibieron tratamientos odontológicos; preventivos 15,0% (21; 144) y curativos 13,0% (18; 144); siendo la mayor patología caries dental. CONCLUSIÓN. Se determinó el perfil demográfico y epidemiológico de los pacientes con Hemofilia y von Willebrand que permitió brindar un tratamiento integral, interdisciplinario y oportuno.

INTRODUCTION. Hereditary abnormalities of hemostasis are rare pathologies, within these are: Hemophilia A, Hemophilia B and von Willebrand. Hemophilia is an inherited disorder, linked to the X chromosome, caused by absence or reduced activity of factor VIII or IX. Von Willebrand's disease is caused by factor VIII deficiency. OBJECTIVE. Determine the demographic and epidemiological profile of patients with hemophilia and von Willebrand. MATERIALS AND METHODS. Observational, descriptive, cross-sectional study. The study population was 133719 with a sample of 144 patients, the inclusion criteria were: patients of both sexes between 2 and 88 years of age, with a diagnosis of Hemophilia A, B, von Willebrand. Attended in the external consultation of the Stomatology Area of the Carlos Andrade Marín Specialty Hospital, in the period 2015-2018. Data obtained from the AS400 system, analyzed in the International Business Machines Statistical Package for the Social Sciences program, Version 22.0. RESULTS 77,0% (111; 144) belonged to the male gender. The age range was between 23 and 33 years with 24,0% (34; 144). They had hemophilia at 62,0% (93; 144); Hemophilia B 6,0% (9; 144); von Willerbrand 28,0% (42; 144). 50,0% (77; 144) received dental treatments; preventive 15,0% (21; 144) and curative 13,0% (18; 144); being the biggest dental caries pathology. CONCLUSION. The demographic and epidemiological profile of patients with Hemophilia and von Willebrand was determined, which allowed to provide a comprehensive, interdisciplinary and timely treatment.

Construction of controllable polyethylene glycol bioactive coating with hemocompatibility from the surface of modified glass substrate / 生物医学工程学杂志

A diblock copolymer, poly(ethylene glycol) methacrylate-block-glycidyl methacrylate (PEGMA-GMA), was prepared on glass substrate by surface-initiated atom transfer radical polymerization (SI-ATRP), and endothelial specific peptide Arg-Glu-Asp-Val (REDV) was immobilized at the end of the PEGMA-GMA polymer brush by ring opening reaction through the rich epoxy groups in the GMA. The structure and hydrophilicity of the polymer brushes were characterized by static water contact angle, X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). The results showed that the REDV modified copolymer brushes were successfully constructed on the glass substrates. The REDV peptide immobilized onto surface was quantitatively characterized by ultraviolet-visible spectroscopy (UV-VIS). The blood compatibility of the coating was characterized by recalcification time and platelet adhesion assay. The results showed that the polymer coating had good blood compatibility. The multifunctional active polymer coating with PEGMA and peptide produced an excellent prospect in surface construction with endothelial cells selectivity.

Refractariedad plaquetaria: acercamiento al diagnóstico / Platelet refractoriness: approaches to diagnostic

La refractariedad plaquetaria representa un problema clínico significativo que complica la transfusión de plaquetas, está asociada con resultados clínicos adversos y elevados costos hospitalarios. Se define como una respuesta inadecuada a la transfusión de plaquetas después de dos transfusiones consecutivas. Las causas no inmunes son las más frecuentes y las primeras que deben ser investigadas en el diagnóstico de refractariedad plaquetaria. La refractariedad de causa inmune está mediada por anticuerpos contra antígenos HLA o HPA. Si se identifican los anticuerpos, existen tres formas de identificar unidades de plaquetas compatibles: el tipaje HLA, la prueba cruzada y la predicción de la especificidad del anticuerpo. Se recomienda el empleo de plaquetas fresca ABO idénticas y fenotipadas para eliminar estas variables potenciales como causa de refractariedad(AU)

Platelet refractoriness represent a significant clinical problem that complicates the provision of platelet transfusions, it is associated with adverse clinical outcomes and increases health care costs. Platelet refractoriness is defined as an inadequate response to platelet transfusions after two sequential transfusions. Nonimmune causes are the most likely and the first that should be explored in the diagnosis of platelet refractoriness. Immune-mediated platelet refractoriness is cause by antibodies to human leukocyte antigens (HLAs) and/or human platelet antigens. If antibodies are identified, there are 3 strategies for identifying compatible platelet units: HLA matching, crossmatching, and antibody specificity prediction. It is recommended to use fresh and ABO-matched platelets in the diagnosis of platelet refractoriness to eliminate these potential variables as causes of refractoriness(AU)

Myr-RKEFAK Peptide Selectively Regulates Outside-in Signaling Transduction-related Functions in Human Platelets / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To study the effect of interaction of the talin rod domain integrin binding site 2 with integrin β3 on platelet signal transduction.</p><p><b>METHODS</b>A peptide that mimics the membrane proximal α helix 6 residues R724 KEFAK729 of the integrin β3 cytoplasmic tails was designed and synthesized, to which the myristoylation was covalently linked to the N-terminal of the peptide enabling membrane penetration. The effects of myr-RKEFAK peptide on the typical platelet outside-in signaling ovent (stable adhesion and spreading on immobilized fibrinogen, aggregation, fibrin clot retraction) and inside-out signaling events (soluble fibrinogen binding) were tested.</p><p><b>RESULTS</b>myr-RKEFAK peptide dose-dependently inhibited platelet stable adhesion and spreading on immobilized fibrinogen, irreversible aggregation, as well as fibrin clot retraction, but not soluble fibrinogen binding and reversible phase of platelet aggregation.</p><p><b>CONCLUSION</b>The cell-penetrating peptide myr-RKEFAK causes an inhibitory effect on integrin β3 outside-in signaling-regulated platelets functions, but did not affect inside-out signaling-regulated platelets functions.</p>

Comparison of platelet adhesion behavior on pure titanium surfaces modified by different techniques / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To evaluate the platelet adhesion ability on pure titanium surfaces modified with different techniques.</p><p><b>METHODS</b>Pure titanium specimens were treated with 5 different surface modification techniques, including machine polish (MP), dual acid-etch (DAE), sand blast-large grit and acid-etch (SLA), micro-arc oxidation (MAO) and anodized titania nanotube (TNT). The surface topographies of specimens were observed by scanning electron microscopy (SEM). Chemical compositions, surface roughness and static water contact angle of specimens were detected by energy dispersive spectrometer (EDS), laser scanning confocal microscope (LSCM) and contact angle analyzer respectively. Platelets were cultured on specimen surfaces for 30 min. The amount and viability of adhered platelets adhered were evaluated. Platelet distribution and morphology were observed by LSCM and SEM.</p><p><b>RESULTS</b>Surface topographies of the five groups of specimens differed significantly. MP, DAE, SLA and MAO surfaces showed micro-scale topographies, while TNT surfaces showed nano-scale topography with nanotubes at the diameter of (80.46 ± 0.35) nm. The surface roughness of MAO was the highest among the 5 groups. TNT surfaces demonstrated the lowest roughness as well as the lowest static water contact angle as 13.55° ± 0.96°. The amount of platelets adhered on TNT surface was the greatest as (300 729 ± 8 325) platelet/µl and the viability was the highest (A450 value 2.14 ± 0.05). Platelet adhered intensively on TNT surfaces, forming pseudopodia, extending and connecting with each other.</p><p><b>CONCLUSIONS</b>Surface properties of pure titanium affect platelet adhesion ability. Nano-scale topography can greatly improve platelet adhesion. Increased surface roughness and hydrophilicity can improve platelet adhesion ability.</p>

Frecuencia del síndrome de plaquetas pegajosas en pacientes con pérdidas fetales recurrentes / Frequency of sticky platelet syndrome in patients with recurrent fetal loss

El síndrome de las plaquetas pegajosas es un trastorno plaquetario autosómico dominante considerado como una de las causas más frecuentes de eventos trombóticos. Se cree que el defecto específico puede estar localizado en los receptores de la superficie plaquetaria y está caracterizado por un incremento anormal en la agregabilidad de las plaquetas con difosfato de adenosina, epinefrina, o ambos. En estudios realizados acerca de esta entidad se ha descrito una elevada incidencia, pero esta se ha calculado en pacientes que han tenido episodios trombóticos previos (enfermedad tromboembólica, infarto agudo del miocardio y accidente cerebrovascular), antecedentes familiares o tienen factores de riesgo para este tipo de eventos, mientras que su incidencia en una población de mujeres en edad fértil, con dos o más pérdidas de embarazo y sin antecedentes es desconocida. En el presente trabajo se estudiaron un total de 126 pacientes femeninas con al menos dos pérdidas de embarazo; de ellas, 27 resultaron positivas al estudio de hipersensibilidad plaquetaria con difosfato de adenosina y epinefrina mediante pruebas de agregometría, lo que representa el 21 por ciento de positividad en la población estudiada. Es significativo que la clase de síndrome de plaqueta pegajosa predominante fue de tipo II (hipersensibilidad con epinefrina). Finalmente, destacar que el seguimiento y tratamiento oportuno durante la gestación en las pacientes incluidas en el estudio ha permitido el nacimiento de 4 niños saludables de madres con síndrome de plaquetas pegajosas...

The sticky platelet syndrome is an autosomal dominant platelet disorder considered one of the most frequent causes of thrombotic events. It is supposed that the specific fault can be localized to the platelet surface receptor and is characterized by an abnormal increase in aggregability adenosine diphosphate and/or epinephrine. In studies on this entity a high incidence has been described, but this was calculated in patients who have had previous thrombotic events (thromboembolic disease, myocardial infarction and stroke), family history or risk factors for this kind of events, while its incidence in a population of women of childbearing age with two or more pregnancy losses and no previous history is unknown.During our research a total of 126 female patients with at least two miscarriages were studied; 27 of them showed platelet hypersensitivity to adenosine diphosphate and epinephrine by testing aggregometry, which represents 21 percent positivity in the population studied. It is significant that the sticky platelet syndrome was predominantly of type II (hypersensitivity with epinephrine). In conclusion, we consider important to remark that with the monitoring and opportune treatment during pregnancy, four of the patients included in our study gave birth four healthy children despite the sticky platelet syndrome...

Hemocompatibility of polyoxymethylene used for bileaflet heart valve / 生物医学工程学杂志

The possibility of polyoxymethylene (POM) as heart valve leaflet material was investigated by comparing the hemocompatibility with that of 316L stainless steel and low-temperature isotropic pyrolytic carbon (LTIC). Surface hydrophobicity was characterized by water contact angle measurement. Platelet adhesion, APTT/PT/TT and hemolysis rate tests were applied for evaluating hemocompatibility. The results showed that POM was hydrophobic and had a low hemolytic rate, adhesion amount and activation degree of platelets on POM surface were less than 316L stainless steel, and was similar to LTIC. This research pointed out potential application of POM as heart valve leaflets.

The infection of microvascular endothelial cells with ExoU-producing Pseudomonas aeruginosa triggers the release of von Willebrand factor and platelet adhesion

An increased plasma concentration of von Willebrand factor (vWF) is detected in individuals with many infectious diseases and is accepted as a marker of endothelium activation and prothrombotic condition. To determine whether ExoU, a Pseudomonas aeruginosa cytotoxin with proinflammatory activity, enhances the release of vWF, microvascular endothelial cells were infected with the ExoU-producing PA103 P. aeruginosa strain or an exoU-deficient mutant. Significantly increased vWF concentrations were detected in conditioned medium and subendothelial extracellular matrix from cultures infected with the wild-type bacteria, as determined by enzyme-linked immunoassays. PA103-infected cells also released higher concentrations of procoagulant microparticles containing increased amounts of membrane-associated vWF, as determined by flow cytometric analyses of cell culture supernatants. Both flow cytometry and confocal microscopy showed that increased amounts of vWF were associated with cytoplasmic membranes from cells infected with the ExoU-producing bacteria. PA103-infected cultures exposed to platelet suspensions exhibited increased percentages of cells with platelet adhesion. Because no modulation of the vWF mRNA levels was detected by reverse transcription-polymerase chain reaction assays in PA103-infected cells, ExoU is likely to have induced the release of vWF from cytoplasmic stores rather than vWF gene transcription. Such release is likely to modify the thromboresistance of microvascular endothelial cells.

Effects of multi-walled carbon nano onions on platelet adhesion and experimental thrombogenesis in rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effects of multi-walled carbon nano-onions (MWCNOs) on platelet adhesion and experimental thrombosis in rats.</p><p><b>METHODS</b>Experimental rats were randomly divided into sham operation group, solvent group, and MWCNO group, each including 6 ∼ 9 rats. An inverted fluorescence microscope and a flow chamber were used to observe the effects of 20 g/ml MWCNOs on platelet adhesion at shear rates of 500 s(-1) and 1000 s(-1); the experiment was repeated at least three times in each group. A rat model of carotid artery thrombosis was induced by 25% FeCl3, and the effects of 2 mg/kg MWCNOs on the blood flow and wet weight of thrombus per millimeter in the model were observed.</p><p><b>RESULTS</b>When the shear rate was 500 s(-1), the MWCNO group showed a significantly smaller number of adhering platelets than the solvent group (58.3 ± 16.1 platelets/0.01 mm(2) vs 190.1 ± 36.0 platelets/0.01 mm(2)), but the inhibitory effect of MWCNOs on platelet adhesion disappeared as the shear rate increased to 1000 s(-1). The wet weights of thrombus per millimeter at 0 h after injection of a solvent or MWCNOs via the caudal vein were 0.83 ± 0.12 mg/mm in the solvent group and 0.97 ± 0.11 mg/mm in the MWCNO group, and the wet weights of thrombus per millimeter at 12 h after injection were 0.89 ± 0.12 mg/mm in the solvent group and 1.01 ± 0.15 mg/mm in the MWCNO group, exhibiting no significant differences between the two groups (P > 0.05). There were also no significant differences between the two groups in terms of blood flow at 0 h and 12 h after injection (P > 0.05).</p><p><b>CONCLUSION</b>MWCNOs have inhibitory effect on platelet adhesion in vitro, but the injection of MWCNOs via the caudal vein has no effects on the blood flow and wet weight of thrombus per millimeter in experimental thrombosis in rats.</p>

Effects of liver sinusoid endothelial cell injury in mouse hepatic veno-occlusive disease / 中国实验血液学杂志

This study was purposed to investigate the role of monocrotaline-inducing mouse liver sinusoid endothelial cell (SEC) injury in hepatic veno-occlusive disease. BALB/c mice were randomly divided into 2 groups: control group and monocrotaline group, mice were orally administrated with normal saline or monocrotaline with concentration of 200 mg/kg at days 0, 1, 2, respectively. At days 3, 4, 6, 8 and 10 after oral administration with normal saline or monocrotaline, the liver function (ALT, TBIL, AKP) and liver index were examined, and the percentage of activated platelets were detected by flow cytometry. The SEC, vascular endothelial cells and hepatic fibrosis were observed by staining with hematoxylin-eosin and Masson. Transmission electron microscopy was used to observe sinusoidal endothelial cell damage and platelet adhesion. The results showed that compared with control group, mice in monocrotaline group were characterized by severe damage of SEC, numbers of platelet aggregation and adhesion, central number and sinusoidal fibrosis. The percentage of activated platelets and liver index increased (P < 0.05). The characterization of portal hypertension was presented later, such as dysfunction of liver and ascites. It is concluded that SEC injury induced by monocrotaline may be the first step of hepatic veno-occlusive disease, and this kind of SEC injury is self-limiting, but fibrosis is always observed.

El síndrome de las plaquetas pegajosas y su diagnóstico en el laboratorio / The sticky platelet syndrome and its diagnosis in the laboratory

El síndrome de las plaquetas pegajosas (SPP) es un trastorno plaquetario autosómico dominante considerado como una de las causas más frecuentes de eventos trombóticos, tanto arteriales como venosos. Este síndrome supone trastornos en la agregación de las plaquetas caracterizados por su incremento anormal. El mecanismo patogénico no se conoce; su existencia puede determinarse con las pruebas de agregación y adhesión plaquetarias. Tampoco se conoce su prevalencia, pero hay datos que sugieren que es frecuente. Algunos investigadores plantean que es responsable del 23 por ciento de las trombosis arteriales inexplicables y del 14 por ciento de las venosas, en las que no es posible identificar una causa. Se presenta una breve revisión acerca de la información disponible sobre el síndrome de las plaquetas pegajosas y su trascendencia en la salud. En Cuba existen pocos reportes de la evaluación clínica de pacientes con esta afección, por lo que resulta necesario realizar estudios más profundos para establecer la magnitud de la enfermedad

The sticky platelet syndrome (SPS) is an autosomal dominant platelet disorder considered as one of the most common causes of thrombotic events, both arterial and venous. This syndrome involves disturbances in platelet aggregation characterized by abnormal increase. The pathogenic mechanism is not known. Its existence can be determined by platelet aggregation and platelet adhesion tests. Its prevalence is also unknown, but evidence suggests that it is common. Some researchers argue that it is responsible for 23 percent of unexplained arterial thrombosis and 14 percent of the vein thrombosis, in which is not possible to identify a cause. Here a brief review on the available information on the sticky platelet syndrome and its importance in health is shown. In Cuba there are few reports of the clinical evaluation of patients with this condition, so further study to determine the extent of the disease is needed

Study of blood compatibility on TiO2 coated biomedical Ni-Ti shape memory alloy / 生物医学工程学杂志

We coated a thin TiO2 film on the surface of Ni-Ti shape memory alloy by activated sputter method in the present work. The blood platelet adherence and antithrombogenicity of the TiO2-coated Ni-Ti alloy were evaluated. The results showed that the platelets on the TiO2-coated Ni-Ti alloy were fewer than those on 316L stainless steel, and no agglomeration or distortion for the platelets on the coated alloy was found, which means less probability of blood coagulation for the alloy. The coagulation time on the coated Ni-Ti shape memory alloy was longer than that on the 316L. Compared with that on the 316L stainless steel, the TiO2 coated Ni-Ti shape memory alloy showed better blood compatibility, indicating that the Ni-Ti alloy with TiO2 coating is a kind of ideal biomedical materials with high clinical value.

The role of amino acid sequence between 551 and 565 in the cytoplasmic domain of glycoprotein (GP) I b alpha in the regulation of the VWF binding to GP I b alpha / 中华血液学杂志

<p><b>OBJECTIVE</b>To explore the role of the amino acids between 551 and 565 in the cytoplasmic domain of glycoprotein (GP) I b alpha in the VWF binding to GP I b alpha.</p><p><b>METHODS</b>The VWF binding to GP I b alpha induced by ristocetin was analyzed by flow cytometry, in three GP I b-IX-expressing Chinese hamster ovary (CHO) cell lines 1b9, delta 565 and delta 551, adhesion of above cells on VWF by flow chamber analysis at shear rate of 200 s(-1). The spread of GP I b-IX-expressing cells were stimulated with botrocetin on VWF-coated coverslips by confocal microscope.</p><p><b>RESULTS</b>The VWF binding to GP I b alpha was higher in delta 565 cells stimulated by ristocetin than in delta 551 or 1b9 cells. The number of delta 565 cells adhered on the VWF-coated-chamber was more than that of controls at shear rate of 200 s(-1). Moreover, the surface spreading areas of delta 565 cells were greater than that of the controls on VWF-coated coverslips.</p><p><b>CONCLUSIONS</b>The amino acids between 551 and 565 in the cytoplasmic domain of GP I b alpha regulates the VWF binding to GP I b alpha.</p>

Research on fibrinogen adsorption and its transformation response in hemocompatibility / 生物医学工程学杂志

In this research,enzyme linked immunoassay (ELISA) was used to assay the fibrinogen (FIG) adsorbed on the Ti-O films and on the low temperature isotropic carbon (LTIC) films which were planted in the femoral arteries of 6 mongrel dogs for six months, respectively. The Ti-O films were planted in the dogs' left femoral arteries; the LTIC films as controls were planted in the dogs' right femoral arteries. The contents adsorbed in these two kinds of films were examined by scanning electron microscopy (SEM). The quantities of FIG adhered or denatured on the Ti-O films or LTIC films determined by ELISA, and the platelets adhered on the two kinds of films examined by SEM were of significant difference between the two groups. In the blood vessel, the amount of FIG adhered on biomaterial was related to its component and construction. FIG released electron to the biomaterial and induced the unfolding of C term of the gamma-chain of FIG, and the conjugation point and effect point were exposed. In conclusion, the biomaterial, which has the capability for resisting the electron release from FIG as well as for maintaining the invariable electric condition, will have excellent hemocompatibility.

Study on anti-coagulant property of radio frequency sputtering nano-sized TiO2 thin films / 生物医学工程学杂志

Nano-TiO2 thin films were prepared by Radio frequency (RF) sputtering on pyrolytic carbon substrates. The influences of sputtering power on the structure and the surface morphology of TiO2 thin films were investigated by X-ray diffraction (XRD), and by scanning electron microscopy (SEM). The results show that the TiO2 films change to anatase through the optimum of sputtering power. The mean diameter of nano-particle is about 30 nm. The anti-coagulant property of TiO2 thin films was observed through platelet adhesion in vitro. The result of experiment reveals the amount of thrombus on the TiO2 thin films being much less than that on the pyrolytic carbon. It also indicates that the RF sputtering Nano-sized TiO2 thin films will be a new kind of promising materials applied to artificial heart valve and endovascular stent.

Study and evaluation on hemocompatibility of biomaterials / 生物医学工程学杂志

Hemocompatibility is an important component of biocompatibility; it reflects the degree of interaction between material and blood. Hemocompatibility is multifaceted, so that the material's impact on the blood and the underlying mechanism are very complicated. This article presents a review of researches probing the impact of material on blood via contact activation and plasma protein adsorption; via the platelet activated and the formation of thrombin; via the complement system activated and the activation of leukocytes as well as other mechanisms of hemolysis. The current methods for evaluation and the future trend of development are also introduced.

Tobacco smoking and surgical healing of oral tissues: a review.

It is believed that the crew of Columbus had introduced tobacco from the 'American India' to the rest of the world, and tobacco was attributed as a medicinal plant. It was often used to avert hunger during long hours of work. But in reality, tobacco causes various ill effects including pre-malignant lesions and cancers. This article aims at reviewing the literature pertaining to the effect of tobacco smoking upon the outcome of various surgical procedures performed in the oral cavity. Tobacco affects postoperative wound healing following surgical and nonsurgical tooth extractions, routine maxillofacial surgeries, implants, and periodontal therapies. In an experimental study, bone regeneration after distraction osteogenesis was found to be negatively affected by smoking. Thus, tobacco, a peripheral vasoconstrictor, along with its products like nicotine increases platelet adhesiveness, raises the risk of microvascular occlusion, and causes tissue ischemia. Smoking tobacco is also associated with catecholamines release resulting in vasoconstriction and decreased tissue perfusion. Smoking is believed to suppress the innate and host immune responses, affecting the function of neutrophils--the prime line of defense against infection. Thus, the association between smoking and delayed healing of oral tissues following surgeries is evident. Dental surgeons should stress on the ill effects of tobacco upon the routine postoperative healing to smoker patients and should aid them to become tobacco-free.