The antimicrobial resistance patterns and associated determinants in Streptococcus suis isolated from humans in southern Vietnam, 1997-2008

Background

Our objective was to determine the frequency and determinants of presentation to care with advanced HIV disease in patients who discover their HIV diagnosis at this stage as well as those with delayed presentation to care after HIV diagnosis in earlier stages.

Methods

We collected data on 1,819 HIV-infected patients in Brussels (Belgium) and Northern France from January 1997 to December 2007. "Advanced HIV disease" was defined as CD4 count <200/mm³ or clinically-defined AIDS at study inclusion and was stratified into two groups: (a) late testing, defined as presentation to care with advanced HIV disease and HIV diagnosis ≤6 months before initiation of HIV care; and (b) delayed presentation to care, defined as presentation to care with advanced HIV disease and HIV diagnosis >6 months before initiation of HIV care. We used multinomial logistic regression to determine the factors associated with delayed presentation to care and late testing.

Results

Of the 570 patients initiating care with advanced HIV disease, 475 (83.3%) were tested late and 95 (16.7%) had delayed presentation to care. Risk factors for delayed presentation to care were: age 30-50 years, injection drug use, and follow-up in Brussels. Risk factors for late testing were: sub-Saharan African origin, male gender, and older age. HIV transmission through heterosexual contact was associated with an increased risk of both delayed presentation to care and late testing. Patients who initiated HIV care in 2003-2007 were less likely to have been tested late or to have a delayed presentation to care than patients who initiated care before 2003.

Conclusion

A considerable proportion of HIV-infected patients present to care with advanced HIV disease. Late testing, rather than a delay in initiating care after earlier HIV testing, is the main determinant of presentation to care with advanced HIV disease. The factors associated with delay presentation to care differ from those associated with late testing. Different strategies should be developed to optimize early access to care in these two groups.     

A case of pulmonary vein obstruction: evaluation using newer echocardiographic imaging techniques

A 59-year-old woman was admitted in our hospital due to persistentcough and dyspnea. Transthoracic 2-dimensional echocardiographydemonstrated a cardiac mass (29x34 mm) that extended from theright upper pulmonary vein into the left atrium causing thepartial obstruction of the right lower vein as indicated bythe increased Doppler velocities. Contrast echocardiographyconfirmed the presence of microcirculation within the mass.During transesophageal (TEE) echocardiographic study, colorDoppler imaging and power Doppler imaging (Angio^® Vivid7, GE Medical System, Horten, Norway) demonstrated the presenceof vascular flow within the mass. A chest magnetic resonancetomography showed a pulmonary mass of 30x25x28 mm infiltratingthe pulmonary veins. After surgery, biopsy confirmed a highgrade mucoepidermoid lung cancer with few large arterioles.The new echocardiographic techniques can reliably differentiatea cardiac tumor from a cardiac thrombus.     

Evidence for a novel gene for familial febrile convulsions, FEB2, linked to chromosome 19p in an extended family from the Midwest

Febrile convulsions are a common form of childhood seizure. It is estimated that between 2 and 5% of children will have a febrile convulsion before the age of 5. It has long been recognized that there is a significant genetic component for susceptibility to this type of seizure. Wallace, Berkovic and co-workers recently reported linkage of a putative autosomal dominant febrile convulsion gene to chromosome 8q13-21. We report here another autosomal dominant febrile convulsion locus on chromosome 19p. Linkage analysis in this large multi- generational family gave a maximum pairwise lod score of 4.52 with marker Mfd120 at locus D19S177. Linkage to the chromosome 8 locus was excluded in this family. Haplotype analysis using both affected and unaffected family members indicates that this febrile convulsion gene, which we call FEB2 , can be localized to an 11.7 cM, 1-2 Mb section of chromosome 19p13.3, between loci D19S591 and D19S395.      

自体血照射回输提高食管癌患者抗辐射的作用

目的探讨自体血液照射回输提高食管癌患者抗辐射能力及对机体正常组织的合理防护．方法食管癌患者６６例随机分为研究组（自体血液照射回输加放疗）和对照组（常规放疗组）．观察两组急性放射性食管炎的发生率及研究组患者血疗前后ＩＬ２，Ｔ淋巴细胞亚群的变化．结果急性放射性食管炎发生率：研究组为１２１％（４／３３），对照组６０６％（２０／３３，Ｐ＜００１）；发生急性放射性食管炎的平均放疗剂量（Ｘ±ＳｃＧＹ）研究组４０５０±８２２，对照组２４６０±６０９（Ｐ＜００１）；研究组血疗前后ＩＬ２，Ｔ淋巴细胞亚群也都有非常显著变化．结论自体血液照射回输可提高食管癌患者抗辐射功能，可能是低剂量辐射刺激诱发机体的适应性和刺激机体的免疫功能，提高了正常组织对放疗的耐受量而不对肿瘤组织起保护作用．     

Inhibitory effect of a fava bean component on the in vitro development of Plasmodium falciparum in normal and glucose-6-phosphate dehydrogenase deficient erythrocytes

We examined the hypothesis that G-6-PD deficiency associated with fava bean ingestion confers resistance to malaria by studying the in vitro interactions between malaria parasites (Plasmodium falciparum), human erythrocytes with varying degrees of G-6-PD deficiency, and isouramil (IU), a fava bean extract that is known to cause oxidant stress and hemolysis of G-6-PD-deficient erythrocytes. Untreated G-6-PD-deficient and normal erythrocytes supported the in vitro growth of P. falciparum equally well. However, after pretreatment with IU, G-6-PD-deficient erythrocytes did not support parasite growth in vitro, whereas growth remained high in normal erythrocytes. Parasite growth was proportional to the G-6-PD activity of the IU-treated erythrocytes. In contrast, when parasitized erythrocytes were exposed to IU, parasites even in normal erythrocytes were destroyed. Ring forms were much less sensitive than late trophozoites and schizonts. The results suggest that there are two modes by which IU affects the development of P. falciparum and demonstrate in vitro that G-6-PD deficiency confers resistance against malaria under conditions of fava-bean-associated oxidant stress.     

Activation of plasminogen by tissue plasminogen activator on normal and thrombasthenic platelets: effects on surface proteins and platelet aggregation

Tissue plasminogen activator (TPA) converts plasminogen to plasmin within the fibrin clot, thus localizing activation of fibrinolysis. To determine the extent to which platelets promote activation of plasminogen by TPA, we studied the interaction of TPA and plasminogen with unstimulated platelets. Normal washed platelets incubated in the presence of physiologic concentrations of plasminogen (180 micrograms/mL) and TPA (20 ng/mL) failed to generate plasmin activity. In contrast, incubation of platelets with TPA concentrations achieved during thrombolytic therapy (40 to 800 ng/mL) produced a tenfold to 50- fold increase in plasmin activity. After exposure to plasminogen and 200 ng/mL of TPA for one hour, platelets failed to agglutinate in the presence of ristocetin. Incubation of platelets suspended in autologous plasma with 400 ng/mL of TPA for one hour also inhibited ristocetin- induced agglutination. Exposure of platelets to plasminogen and increasing concentrations of TPA correlated with a decrease in glycoprotein Ib (GPIb) and an increase in glycocalicin, as shown by immunoblotting. The glycoprotein IIb/IIIa (GPIIb/IIIa) complex and a 250,000-dalton protein also disappeared from washed platelets after incubation with plasminogen and 200 ng/mL of TPA for one hour. These platelets failed to aggregate in the presence of adenosine diphosphate (ADP) or gamma thrombin, although aggregation in response to calcium ionophore A23187 and arachidonic acid remained intact. However, aggregation in response to all four agonists was normal when platelets were incubated with TPA in the presence of autologous plasma. Platelets from a patient with Glanzmann's thrombasthenia also generated plasmin in the presence of TPA. Hydrolysis of GPIb and inhibition of ristocetin- induced agglutination occurred to a lesser extent with these platelets than with control platelets. We conclude that platelets provide a surface for activation of plasminogen by pharmacologic amounts of TPA. Plasmin generation leads to degradation of GPIb and decreased ristocetin-induced agglutination in normal and thrombasthenic platelets, as well as degradation of GPIIb/IIIa in normal washed platelets and inhibition of ADP and gamma thrombin-induced aggregation. These findings suggest that pharmacologic concentrations of TPA may cause platelet dysfunction due to plasmin generation on the platelet surface.     

Spectrin oxidation correlates with membrane vesiculation in stored RBCs

An increase in spectrin oxidation in a variety of erythrocytes displaying a tendency to vesiculate has been previously described. To explore this relationship in more detail, we have studied blood stored in citrate-phosphate-dextrose-adenine under blood bank conditions because, in this system, vesiculation occurs slowly. Vesiculation was quantitated by measuring acetylcholinesterase release, and the extent of spectrin oxidation was detected by using thiol-disulfide exchange chromatography. A strong correlation (r = .92) was found between the extent of spectrin oxidation and vesiculation when blood from five donors was analyzed at weekly intervals during storage. This strongly suggests that spectrin oxidation plays a role in the formation of spectrin-free vesicles, thereby limiting the shelf life of stored blood.