Abstract-A novel method for Brillouin gain spectrum measurements in optical fibers is presented. It is based on the pump and probe technique with the specificity to use a single laser source together with an external modulator to generate the interacting lightwaves. The high accuracy and inherent stability of the technique makes it suitable for calibration and reference measurements. Different fibers with different refractive index profiles have been tested and characterized. The problem of the evolution of the polarization of the interacting waves is addressed in the article and a polarization insensitive determination of the actual Brillouin gain coefficient is made possible through two successive measurements with different polarizations. The effects of strain and temperature on the Brillouin gain spectrum are also fully characterized.Index Terms-Brillouin scattering, optical fiber measurements, optical fiber scattering, strain measurements, temperature measurements.

T cell activation requires that the cell meet increased energetic and biosynthetic demands. We showed that exogenous nutrient availability regulated the differentiation of naïve CD4(+) T cells into distinct subsets. Activation of naïve CD4(+) T cells under conditions of glutamine deprivation resulted in their differentiation into Foxp3(+) (forkhead box P3-positive) regulatory T (Treg) cells, which had suppressor function in vivo. Moreover, glutamine-deprived CD4(+) T cells that were activated in the presence of cytokines that normally induce the generation of T helper 1 (TH1) cells instead differentiated into Foxp3(+) Treg cells. We found that α-ketoglutarate (αKG), the glutamine-derived metabolite that enters into the mitochondrial citric acid cycle, acted as a metabolic regulator of CD4(+) T cell differentiation. Activation of glutamine-deprived naïve CD4(+) T cells in the presence of a cell-permeable αKG analog increased the expression of the gene encoding the TH1 cell-associated transcription factor Tbet and resulted in their differentiation into TH1 cells, concomitant with stimulation of mammalian target of rapamycin complex 1 (mTORC1) signaling. Together, these data suggest that a decrease in the intracellular amount of αKG, caused by the limited availability of extracellular glutamine, shifts the balance between the generation of TH1 and Treg cells toward that of a Treg phenotype.