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    ABSTRACT: Leprosy (Hansen's disease) is a chronic granulomatous infection caused by Mycobacterium leprae with peripheral neuropathy as cutaneous and neurological manifestations. Peripheral nerve regeneration may be stimulated by vascular endothelial growth factor and other growth factors (GFs) that have important roles in extracellular matrix regeneration. All of those GFs can be found in platelet-rich plasma (PRP) preparation. The effect of PRP injection in leprosy peripheral neuropathy has never been reported. A double-blind, randomized, control clinical trial was conducted among 60 patients with leprosy peripheral neuropathy. They were randomized to receive either a 1-ml injection of PRP as treatment or a 1-ml injection of platelet-poor plasma (PPP) as control. Skin sensibilities were measured by two-point discrimination test (TPDT) and visual analog scale (VAS), which were taken before and two weeks after treatment. Perineural injection of PRP was shown to be significantly more effective than PPP (P < 0.05) either in VAS or TPDT measurements. In both groups, the patients had a tingling sensation at the time of injection that disappeared shortly after. This study shows that perineural PRP injection could promote improvement of peripheral neuropathy sensibility in patients with leprosy. More research is needed to better determine the effects of PRP in nerve regeneration.
    International journal of dermatology 10/2013;
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    ABSTRACT: Previously, we reported that minocycline, kanamycin and norfloxacin improved the survival rate in the E32511 model that we developed (Infect. Immun. 62: 3447-3453, 1994), but fosfomycin did not. In this study, we investigated the effectiveness of azithromycin (AZM) against Stx2d-producing EHEC O91:H21 strain B2F1 or Stx2c-producing Escherichia coli strain E32511 treated with Mitomycin C in vivo. Recently, we reported the effectiveness of AZM in our model and AZM strongly inhibited the release of Stx2c from E32511 in vitro (PLOS ONE e58959, 2013). However, it was very difficult to completely eliminate E32511 in the mouse feces by treatment with AZM alone. In this report, only AZM or Daio effectively promoted survival of mice infected with B2F1 compared to untreated mice. Furthermore, Daio inhibited the colonization of GFP-expressing B2F1 in the mouse intestine. Similarly, a combination of AZM and Daio in the E32511-infected mice reduced E32511 in the mouse feces and significantly improved survival.
    Microbial Pathogenesis 10/2013;
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    ABSTRACT: A large outbreak of Shiga toxin (Stx)-producing enteroaggregative Escherichia coli (EAEC) O104:H4 occurred in northern Germany. From this outbreak, at least 900 patients developed hemolytic uremic syndrome (HUS), resulting in more than 50 deaths. Thirty percent of the HUS patients showed encephalopathy. We previously established a mouse model with encephalopathy associated with blood brain barrier (BBB) damage after oral infection with the Shiga toxin (Stx) 2c-producing Escherichia coli O157: H- strain E32511 (E32511). In this model, we detected high expression of the Stx receptor synthase enzyme, glycosphingolipid globotriaosylceramide (Gb3) synthase, in endothelial cells (ECs) and neurons in the reticular formation of the medulla oblongata by in situ hybridization. Caspase-3 was activated in neurons in the reticular formation of the medulla oblongata and the anterior horn of the spinal cord. Astrocytes (ASTs) were activated in the medulla oblongata and spinal cord, and a decrease in aquaporin 4 around the ECs suggested that BBB integrity was compromised directly by Stx2c or through the activation of ASTs. We also report the effectiveness of azithromycin (AZM) in our model. Moreover, AZM strongly inhibited the release of Stx2c from E32511 in vitro.
    PLoS ONE 03/2013; 8(3).


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Computer Science and Information Technology (ICCSIT), 2010 3rd IEEE International Conference on; 08/2010

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