Semiconductor laser with extended cavity and intracavity atomic filter.

We report on peculiar dynamic features of laser oscillation in a cavity with a semiconductor junction as the gain medium and an intracavity atomic absorber. The output face of the semiconductor is antireflection coated, and lasing action is achieved by using a diffraction grating to close the laser cavity. The spectral analysis of the laser emission evidences a stable emission with narrow linewidth when the oscillating frequency is resonant with the atomic absorber. We also observe frequency bistability and instability. The change between these regimes is controlled through the bias current in a very reproducible way.

Inducing mutations in the mouse genome with the chemical mutagen ethylnitrosourea.

When compared to other model organisms whose genome is sequenced, the number of mutations identified in the mouse appears extremely reduced and this situation seriously hampers our understanding of mammalian gene function(s). Another important consequence of this shortage is that a majority of human genetic diseases still await an animal model. To improve the situation, two strategies are currently used: the first makes use of embryonic stem cells, in which one can induce knockout mutations almost at will; the second consists of a genome-wide random chemical mutagenesis, followed by screening for mutant phenotypes and subsequent identification of the genetic alteration(s). Several projects are now in progress making use of one or the other of these strategies. Here, we report an original effort where we mutagenized BALB/c males, with the mutagen ethylnitrosourea. Offspring of these males were screened for dominant mutations and a three-generation breeding protocol was set to recover recessive mutations. Eleven mutations were identified (one dominant and ten recessives). Three of these mutations are new alleles (Otop1mlh, Foxn1sepe and probably rodador) at loci where mutations have already been reported, while 4 are new and original alleles (carc, eqlb, frqz, and Sacc). This result indicates that the mouse genome, as expected, is far from being saturated with mutations. More mutations would certainly be discovered using more sophisticated phenotyping protocols. Seven of the 11 new mutant alleles induced in our experiment have been localized on the genetic map as a first step towards positional cloning.

Inducing mutations in the mouse genome with the chemical mutagen ethylnitrosourea

When compared to other model organisms whose genome is sequenced, the number of mutations identified in the mouse appears extremely reduced and this situation seriously hampers our understanding of mammalian gene function(s). Another important consequence of this shortage is that a majority of human genetic diseases still await an animal model. To improve the situation, two strategies are currently used: the first makes use of embryonic stem cells, in which one can induce knockout mutations almost at will; the second consists of a genome-wide random chemical mutagenesis, followed by screening for mutant phenotypes and subsequent identification of the genetic alteration(s). Several projects are now in progress making use of one or the other of these strategies. Here, we report an original effort where we mutagenized BALB/c males, with the mutagen ethylnitrosourea. Offspring of these males were screened for dominant mutations and a three-generation breeding protocol was set to recover recessive mutations. Eleven mutations were identified (one dominant and ten recessives). Three of these mutations are new alleles (Otop1mlh, Foxn1sepe and probably rodador) at loci where mutations have already been reported, while 4 are new and original alleles (carc, eqlb, frqz, and Sacc). This result indicates that the mouse genome, as expected, is far from being saturated with mutations. More mutations would certainly be discovered using more sophisticated phenotyping protocols. Seven of the 11 new mutant alleles induced in our experiment have been localized on the genetic map as a first step towards positional cloning.

Dosagem plasmatica dos acidos biliares conjungados na hepatopatia cronica esquistossomotica. / Plasma levels of conjugated bile acids in chronic schistosomal liver diseases

A concentracao de 2 acidos biliares conjugados, a colilglicina(CG) e a sulfolitocolilglicina(SLCG), foi determinada atraves de RIE no sangue periferico de pacientes portadores de hepatopatia cronica esquistossomotica e cirrose hepatica.Nos pacientes esquistossomoticos, forma hepatointestinal (HI) observou-se uma tendencia a reducao nos niveis plasmaticos da SLCG.A media de valores obtida para a dosagem da CG com o paciente em jejum apresentou especial utilidade na distincao entre as fases compensada e descompensada da esquistossomose hepatesplenica (HE) e da cirrose hepatica. Ja a dosagem pos-prandial da CG, alem de ter sido a determinacao bioquimica que demonstrou maior percentagem de valorea anormais, foi a unica a apresentar media de valores significativamente diferentes entre as formas HI e HE compensada e descompensada, embora falhasse em diferenciar as fases compensada e descompensada da cirrose hepatica. Se os resultados obtidos para CG pos-prandial na hepatopatia esquistossomotica estao relacionados diretamente a uma disfuncao hepatocelular ou a fatores extra-hepaticos, ainda resta a ser estabelecido