ABSTRACT
In order to study the infectious agents causing human disseminated cryptococcosis in the state of Pará, North Brazil, 56 isolates of Cryptococcusspp. (54 isolated from cerebral spinal fluid and two from blood cultures) from 43 cases diagnosed between 2003-2007 were analysed. The species were determined through morphological and physiological tests and genotypes were determined by URA5-RFLP and PCR-fingerprinting (wild-type phage M13). The following species and genotypes were identified: Cryptococcus neoformans VNI (28/56, 50 percent), Cryptococcus gattii VGII (25/56, 44.64 percent) and C. gattii VGI (3/56, 5.26 percent). The genotype VNI occurred in 12 out of 14 HIV-positive adults, whereas the genotype VGII occurred in 11 out of 21 HIV-negative adults (p < 0.02, OR = 6.6 IC95 percent 0.98-56.0). All patients less than 12 years old were HIV negative and six cases were caused by the VGII genotype, one by the VGI and one by VNI. Therefore, endemic primary mycosis in HIV-negative individuals, including an unexpectedly high number of children, caused by the VGII genotype deserves further study and suggests the need for surveillance on cryptococcal infection in the state of Pará, Eastern Amazon.
Subject(s)
Adult , Child , Female , Humans , Male , Cryptococcosis/epidemiology , Cryptococcus/genetics , Endemic Diseases , Brazil/epidemiology , Cryptococcosis/microbiology , Cryptococcus/classification , Cryptococcus/isolation & purification , DNA, Fungal/analysis , Genotype , Mycological Typing Techniques/methods , Polymerase Chain Reaction , Polymorphism, Restriction Fragment LengthABSTRACT
Neurotoxicity induced by methylmercury (MeHg) increases the formation of reactive radicals and accelerates free radical reactions. This review summarizes recent findings in the MeHg-induced formation of free radicals and the role of oxidative stress in its neurotoxicity. Oxidative stress on CNS can produce damage by several interacting mechanisms, including mitochondrial damage with increase in intracellular free Ca(2+), activation and inhibition of enzymes, release of excitatory amino acids, metallothioneins expression, and microtubule disassembly. The nature of antioxidants is discussed and it is suggested that antioxidant enzymes and others antioxidants molecules may protect the central nervous system against neurotoxicity caused by MeHg.
Subject(s)
Animals , Antioxidants/metabolism , Humans , Methylmercury Compounds/toxicity , Nervous System/drug effects , Oxidative StressABSTRACT
The study of neurotransmitter release using aggregate cell cultures has been limited by the fact that cell aggregates are obtained only when cells are maintained in suspension with rotatory agitation. In this report we describe a simple and easy method that uses aggregate cell cultures to study the release of neurotransmitters. The results demonstrate that this relatively simple technique can be of great value to address the problem of neurotransmitter release and study the mechanisms of action of natural and synthetic compounds on the differentiation of functional synapses in the CNS.