Complicaciones de la otitis media con parálisis del sexto par craneal contralateral en pediatría

Otitis media is a frequent infection during childhood. Complications may be present in up to 4 of 100 children including serious neurological complications, particularly in developing countries.We report the case of a 9-year-old girl with no disease history who presented with otitis media, otorrhea, intracranial hypertension syndrome, and paralysis of the VI cranial nerve contralateral to the lesion. A computed tomography scan of the skull and a brain magnetic resonance imaging revealed chronic otomastoiditis, petrous apicitis, and thrombosis of the transverse and sigmoid sinus, the jugular bulb, and the right internal jugular vein. She received antibiotics and surgical treatment.This case shows the spectrum of intra and extracranial complications associated with acute otitis media in the antibiotic era. The physical examination allows early identification of intracranial hypertension with signs such as papilledema and sixth contralateral nerve palsy as an unusual finding.     

Role of sulfatide in normal and pathological cells and tissues

Sulfatide is 3-O-sulfogalactosylceramide that is synthesized by two transferases (ceramide galactosyltransferase and cerebroside sulfotransferase) from ceramide and is specifically degraded by a sulfatase (arylsulfatase A). Sulfatide is a multifunctional molecule for various biological fields including the nervous system, insulin secretion, immune system, hemostasis/thrombosis, bacterial infection, and virus infection. Therefore, abnormal metabolism or expression change of sulfatide could cause various diseases. Here, we discuss the important biological roles of sulfatide in the nervous system, insulin secretion, immune system, hemostasis/thrombosis, cancer, and microbial infections including human immunodeficiency virus and influenza A virus. Our review will be helpful to achieve a comprehensive understanding of sulfatide, which serves as a fundamental target of prevention of and therapy for nervous disorders, diabetes mellitus, immunological diseases, cancer, and infectious diseases.     

Investigations of human platelet-type 12-lipoxygenase: role of lipoxygenase products in platelet activation

Human platelet-type 12-lipoxygenase (12-LOX) has recently been shown to play an important role in regulation of human platelet function by reacting with arachidonic acid (AA). However, a number of other fatty acids are present on the platelet surface that, when cleaved from the phospholipid, can be oxidized by 12-LOX. We sought to characterize the substrate specificity of 12-LOX against six essential fatty acids: AA, dihomo-γ-linolenic acid (DGLA), eicosapentaenoic acid (EPA), α-linolenic acid (ALA), eicosadienoic acid (EDA), and linoleic acid (LA). Three fatty acids were comparable substrates (AA, DGLA, and EPA), one was 5-fold slower (ALA), and two showed no reactivity with 12-LOX (EDA and LA). The bioactive lipid products resulting from 12-LOX oxidation of DGLA, 12-(S)-hydroperoxy-8Z,10E,14Z-eicosatrienoic acid [12(S)-HPETrE], and its reduced product, 12(S)-HETrE, resulted in significant attenuation of agonist-mediated platelet aggregation, granule secretion, αIIbβ3 activation, Rap1 activation, and clot retraction. Treatment with DGLA similarly inhibited PAR1-mediated platelet activation as well as platelet clot retraction. These observations are in surprising contrast to our recent work showing 12(S)-HETE is a prothrombotic bioactive lipid and support our hypothesis that the overall effect of 12-LOX oxidation of fatty acids in the platelet is dependent on the fatty acid substrates available at the platelet membrane.     

The influence of Annexin32, a new Ca2+-dependent phospholipid-binding protein, on coagulation time and thrombosis

The pharmacodynamics of Annexin32, a new Ca2+-dependent phospholipid-binding protein, was studied by measuring coagulation time in rabbits and venous thrombosis in rabbits and rats. Rabbits and rats were given Annexin32 by intravenous administration. Then Kaolin partial thromboplastin time (KPTT), thrombosis in vitro and in vivo were assayed. The results showed that KPTT of rabbits was prolonged (p < 0.01), and the length and weight of thrombus in vitro were reduced (p < 0.01) after administration of Annexin32 at 1 mg/kg. It also inhibited thrombosis in vivo and reduced the weight of venous thrombus significantly in rats (p < 0.01). All these results suggested that Annexin32 possesses the characteristic of antithrombotic effect and fewer side effects on coagulation time.     

血栓通注射液联合利伐沙班预防下肢骨折术后下肢深静脉血栓形成疗效及对患者血液流变学的影响

目的:探讨血栓通注射液联合利伐沙班预防下肢骨折术后下肢深静脉血栓(DVT)形成的疗效及对患者血液流变学的影响。方法:选取2012年4月到2015年7月西安医学院第一附属医院收治的125例下肢骨折术后患者,随机分为对照组63例和观察组62例,对照组患者给予血栓通治疗,观察组患者在对照组的基础上给予利伐沙班治疗。观察两组治疗前后DVT发生率、血清D-二聚体(DD)、同型半胱氨酸(Hcy)以及高敏C-反应蛋白(hs-CRP)、血液流变学指标包括红细胞压积(HTC)、全血黏度(WBV)和纤维蛋白原的变化以及用药安全性。结果:术后3周,观察组DVT的总发生率为9.7%(6例),显著低于对照组的44.4%(28例),差异具有统计学意义(P0.05)。治疗后,两组患者的血清DD、Hcy、hs-CRP、HTC、WBV以及纤维蛋白原水平均较治疗前明显降低(P0.05),且观察组该6个指标显著低于对照组,差异均具有统计学意义(P0.05)。此外,观察组的不良反应发生率为9.68%,对照组为7.94%,两组间比较无明显差异(P0.05)。结论:血栓通注射液联合利伐沙班可有效减少DVT的发生并改善患者的血液高凝状态,是一种预防下肢骨折术后DVT形成的有效方案。     

导管接触溶栓与机械辅助吸栓治疗急性髂股静脉血栓的对比研究

目的:评价导管接触溶栓与机械辅助吸栓治疗急性髂股静脉血栓的临床效果。方法:回顾性分析162例急性下肢深静脉血栓(髂股静脉血栓)形成患者临床资料,其中导管溶栓治疗组(A组)80例、机械辅助吸栓组(B组)82例,比较两组患者治疗后患肢深静脉溶栓率、消肿率、并发症发生率、治疗时间的差异。结果:急性下肢髂股静脉血栓溶栓率B组(46.45±11.56)%显著高于A组(32.05±10.7)%(P0.05)。患肢消肿率B组(68.68±10.75)%和A组(41.34±11.26)%有明显统计学差异(P0.05)。两组并发症发生率无明显统计学意义。两组溶栓时间A组明显长于B组,两组间比较有明显统计学差异。结论:机械辅助吸栓治疗急性髂股静脉血栓早期疗效好于导管接触溶栓。     

Zebrafish model of photochemical thrombosis for translational research and thrombolytic screening in vivo

Acute thromboembolic diseases remain the major global cause of death or disability. Although an array of thrombolytic and antithrombotic drugs has been approved to treat or prevent thromboembolic diseases, many more drugs that target specific clotting mechanisms are under development. Here a novel zebrafish model of photochemical thrombosis is reported and its prospective application for the screening and preclinical testing of thrombolytic agents in vivo is demonstrated. Through photochemical excitation, a thrombus was induced to form at a selected section of the dorsal aorta of larval zebrafish, which had been injected with photosensitizers. Such photochemical thrombosis can be consistently controlled to occlude partially or completely the targeted blood vessel. Detailed mechanistic tests indicate that the zebrafish model of photochemical thrombosis exhibits essential features of classical coagulation and a thrombolytic pathway. For demonstration, tissue plasminogen activator (tPA), a clinically feasible thrombolytic agent, was shown to effectively dissolve photochemically induced blood clots. In light of the numerous unique advantages of zebrafish as a model organism, our approach is expected to benefit not only the development of novel thrombolytic and antithrombotic strategies but also the fundamental or translational research targeting hereditary thrombotic or coagulation disorders.

     

t-plasminogen activator inhibitor-1 polymorphism in idiopathic pulmonary arterial hypertension

AIM:

The aim of the present study was to identify the possible genotypic association of 3’UTR Hind III polymorphism of Plasminogen activator Inhibitor-1 (PAI-1) gene with idiopathic pulmonary arterial hypertension (IPAH).

BACKGROUND:

IPAH is a disorder with abnormally raised mean pulmonary arterial pressure and increase in the resistance to blood flow in pulmonary artery. One of the pathological features seen is development of intraluminal thrombin deposition leading to thrombosis. Plasminogen activator inhibitor-1 is an important inhibitor of the fibrinolytic system; its up-regulation may suppress fibrinolysis and result in an increased risk of thrombosis.

METHOD:

Blood samples from 54 IPAH patients and 100 healthy voluntary donors were analyzed by PCR-RFLP method for 3’UTR Hind III polymorphism.

RESULTS AND DISSCUSSION:

A significant association of Hd2 allele with the disease was observed. Raised mean level of right ventricular systolic pressure was observed in the Hd2/Hd2 genotypic patients, strengthening the role of Hd2 allele in the disease progression. Our data suggests an association of Hd2/Hd2 genotype, which may lead to the up-regulation of PAI-1 gene leading to increased levels of PAI-1, which is seen in IPAH. PAI-1 competes with plasminogen activators and hinders the normal mechanism of plasminogen activation system and leads to thrombosis and formation of plexiform lesions in the lung tissue, further strengthening its role in tissue remodeling and disease progression.