RESUMO
Metformin (MET) is widely used in the treatment of diabetes either alone or in combination with other drugs, in drug discovery to evaluate the anti-diabetic potential of other drugs, and usually as a comparison compound in pharmacokinetics/pharmacodynamics studies. Measuring the concentration of this substance is very important both pre-clinically in different species and clinically in the medical monitoring of diabetic patients to prevent toxicity and ensure adherence to described drugs. Therefore, it is very important to develop a sensitive and selective method to measure MET. In this work, a new electrochemical biosensor based on a carbon paste electrode, modified with bacterial nanocellulose, copper oxide, and silver nanoparticles (Ag NPs/Cu2O/CuO/BNC/CPE) was used for high-sensitivity MET determination. The morphology and structure of this bio-nanocomposite were characterized by ATR-IR, FE-SEM, EDS, mapping, XRD, and DRS techniques. Compared with the CPE electrode, the Ag NPs/Cu2O/CuO/BNC/CPE modified electrode showed much higher electrocatalytic activities toward the oxidation of MET. The measurements were carried out by the cyclic voltammetry technique. Surface conductance was evaluated using the impedance technique. The results showed an increase in surface conductivity. The detection limit was obtained at 42.3 nM and two linear ranges 0.1-76 and 76-1000.0 µM were observed. The developed sensor had good features such as high sensitivity, reproducibility and repeatability, low detection limit, and fast response time. The obtained results from the real sample (MET tablets) were completely satisfactory.
Assuntos
Nanopartículas Metálicas , Metformina , Humanos , Cobre , Reprodutibilidade dos Testes , Prata , Carbono , EletrodosRESUMO
With the completion of the Drosophila genome sequence, an important next step is to extract its biological information by systematic functional analysis of genes. We have produced a high-resolution genetic map of cytological region 38 of Drosophila using 41 deficiency stocks that provide a total of 54 breakpoints within the region. Of a total of 45 independent P-element lines that mapped by in situ hybridization to the region, 14 targeted 7 complementation groups within the 38 region. Additional EMS, X-ray, and spontaneous mutations define a total of 17 complementation groups. Because these two pools partially overlap, the completed analysis revealed 21 distinct complementation groups defined by point mutations. Seven additional functions were defined by trans-heterozygous combinations of deficiencies, resulting in a total of 28 distinct functions. We further produced a developmental expression profile for the 760 kb from 38B to 38E. Of 135 transcription units predicted by GENSCAN, 22 have at least partial homology to mobile genetic elements such as transposons and retroviruses and 17 correspond to previously characterized genes. We analyzed the developmental expression pattern of the remaining genes using poly(A)(+) RNA from ovaries, early and late embryos, larvae, males, and females. We discuss the correlation between GENSCAN predictions and experimentally confirmed transcription units, the high number of male-specific transcripts, and the alignment of the genetic and physical maps in cytological region 38.
Assuntos
Mapeamento Cromossômico , Drosophila/genética , Genoma , Animais , Sequência de Bases , Northern Blotting , Southern Blotting , Bases de Dados como Assunto , Etiquetas de Sequências Expressas , Teste de Complementação Genética , Heterozigoto , Modelos Genéticos , Dados de Sequência Molecular , Mutação , Mapeamento Físico do Cromossomo , Mutação Puntual , Poli A , SoftwareRESUMO
The aim of this study was to investigate the effect of pre-irradiation with microwaves on the induction of radioadaptive response. In the 1(st) phase of the study, 110 male mice were divided into 8 groups. The animals in these groups were exposed/sham-exposed to microwave, low dose rate gamma or both for 5 days. On day six, the animals were exposed to a lethal dose (LD). In the 2(nd) phase, 30 male rats were divided into 2 groups of 15 animals. The 1(st) group received microwave exposure. The 2(nd) group (controls) received the same LD but there was no treatment before the LD. On day 5, all animals were whole-body irradiated with the LD. Statistically significant differences between the survival rate of the mice only exposed to lethal dose of gamma radiation before irradiation with a lethal dose of gamma radiation with those of the animals pre-exposed to either microwave (p=0.02), low dose rate gamma (p=0.001) or both of these physical adapting doses (p=0.003) were observed. Likewise, a statistically significant difference between survival rates of the rats in control and test groups was observed. Altogether, these experiments showed that exposure to microwave radiation may induce a significant survival adaptive response.
RESUMO
BACKGROUND: Transgenic mice are the product of the microinjection of foreign DNA directly into the pronuclei of a one-cell embryo. The foreign DNA can cause insertional inactivation or activation of the flanking genetic locus. EXPERIMENTAL DESIGN: We isolated five lines of transgenic mice harboring the chicken alpha-actin vascular smooth muscle enhancer/promoter linked to the polyomavirus middle T antigen using a standard microinjection protocol. The expression of the transgene was assessed in RNA prepared from affected and nonaffected tissue by RNase protection and reverse transcriptase-polymerase chain reaction analyses. Cell morphology was determined in stained sections from fixed tissues. RESULTS: In this article, we document the development of epithelial hyperplasia in the rectum and distal stomach together with female infertility in a single line of transgenic mice harboring the transgene. We were unable to demonstrate the expression of the transgene in any tissue examined, regardless of the degree of hyperplasia. The phenotype was present in the heterozygous state in both males and females. CONCLUSIONS: In the absence of the expression of the transgene, we conclude that the insertion of the transgene may have caused the epithelial hyperplasia directly or may have contributed to a condition that promotes hyperplasia. The transgene may have activated a dominant-acting neighboring gene.
Assuntos
Actinas/genética , Antígenos Transformantes de Poliomavirus/genética , Transformação Celular Neoplásica/genética , Mucosa Gástrica/patologia , Mucosa Intestinal/patologia , Animais , Sequência de Bases , Clonagem Molecular , Feminino , Hiperplasia/genética , Infertilidade Feminina/genética , Masculino , Camundongos , Camundongos Mutantes , Camundongos Transgênicos , Dados de Sequência Molecular , Músculo Liso/química , Reação em Cadeia da Polimerase , Regiões Promotoras Genéticas/genética , Reto/patologiaRESUMO
Sam68 is a member of a growing family of RNA-binding proteins that contains an extended K homology (KH) domain embedded in a larger domain called the GSG (GRP33, Sam68, GLD1) domain. To identify GSG domain family members, we searched data bases for expressed sequence tags encoding related portions of the Sam68 KH domain. Here we report the identification of two novel Drosophila KH domain proteins, which we termed KEP1 (KH encompassing protein) and SAM. SAM bears sequence identity with mammalian Sam68 and may be the Drosophila Sam68 homolog. We demonstrate that SAM, KEP1, and the recently identified Drosophila Who/How are RNA-binding proteins that are able to self-associate into homomultimers. The GSG domain of KEP1 and SAM was necessary to mediate the RNA binding and self-association. To elucidate the cellular roles of these proteins, SAM, KEP1, and Who/How were expressed in mammalian and Drosophila S2 cells. KEP1 and Who/How were nuclear and SAM was cytoplasmic. The expression of KEP1 and SAM, but not Who/How, activated apoptotic pathways in Drosophila S2 cells. The identification of KEP1 and SAM implies that a large GSG domain protein family exists and helps redefine the boundaries of the GSG domain. Taken together, our data suggest that KEP1 and SAM may play a role in the activation or regulation of apoptosis and further implicate the GSG domain in RNA binding and oligomerization.