Although there are distinct advantages to MgC-GEP, there are also two limitations: MgC-GEP does not determine the absolute expression level of transcripts but the relative abundance of selected transcripts, and the sensitivity of MgC-GEP depends on number of clones sequenced, thus detection of rare transcripts would sequence more clones which will increase the cost. In conclusion, MgC-GEP adopts covnentional RT-PCR, restriction enzyme digestion, concatemer ligation, bacterial transforma- tion and DNA sequencing to assess mRNA profiles without using high-throughput expensive methodologies such as microarray hybridization or deep sequencing. No specific equipment is required in this method. This strategy could be of great benefit for labs with limited funds or limited access to microarray or next-generation sequencing facilities. Thus, MgC-GEP should be a potentially powerful tool for multigene expression profiling in different tissues, during development, or during specific pathologies in both basic and pharmaceutical research. The dysbindin-1 gene was originally identified as a gene associated with schizophrenia through its linkage to chromosome 6p. Several subsequent Chloroprocaine hydrochloride studies have replicated the association between this locus and schizophrenia. In addition, two recent and independent reports have linked certain dysbindin-1 risk haplotypes with bipolar disorder. Dysbindin-1 is widely distributed in the brain, and has been detected both pre- and post-synaptically. A recent immunoelectron microscopy study further revealed that, in the hippocampus, dysbindin-1 is located in synaptic vesicles of axospinous terminals in the dentate gyrus inner molecular layer and CA1 stratum radiatum and in postsynaptic densities and microtubules of dentate hilus neurons and CA1 pyramidal cells. To date, no amino acid sequence mutation in the dysbindin-1 protein that might contribute to the risk of major psychosis has been identified. Furthermore, several studies have implicated the involve- ment of many different alleles and KX1-004 haplotypes as susceptibility variants. These polymorphisms, however, may modulate dysbindin-1 expression levels since reduced dysbindin message and/or protein levels have been found in schizophrenic brains such as prefrontal cortex and hippocampal formation, brain areas commonly affected by the disorder. In the hippocampus of schizophrenic patients, dysbindin-1 reductions occur in the synaptic terminal fields of glutamatergic neurons, especially those located in the DGiml. Although its function in the brain is still not well understood, it may play a role in both glutamatergic and dopaminergic neurotransmission. For example, knockdown of endoge- nous dysbindin with siRNA has been shown to reduce glutamate levels in cultured neurons, suggesting that a decrease in dysbindin levels has synaptic consequences. Furthermore, altered dysbindin-1 expression may contribute to cognitive impairments prominent in schizophrenia, including deficits in attention, memory and executive function. More recently, ‘‘sandy’’ mice, spontaneously occurring dysbindin null mice, have been shown to exhibit a number of behavioral abnormalities associated with reductions in forebrain dopamine transmission. Leptospirosis is an acute febrile illness caused by pathogenic species belonging to the genus Leptospira. This zoonotic disease has a worldwide distribution but is most common in tropical and subtropical regions and has the greatest impact on public health in developing countries. Disease is maintained by chronic carrier hosts that excrete the organism into the environment, and infection in man results from direct contact with infected animals or indirect contact with a contaminated environment.