Magnetometry based on the effect of laser-induced plasmas in a sodium-containing environment.

The magneto-optical resonance response of sodium atoms generated by a high-energy solid-state pulse Nd:YAG laser is studied in different external magnetic fields. We investigate the resonance fluorescence signal of sodium atoms in a simulated sea fog environment based on the laser-induced plasma (LIP) effect. By ionizing an NaCl solution spray to generate sodium atoms in an atmospheric environment, we build a Bell-Bloom magneto-optical resonance system under laboratory conditions. With the help of laser-induced breakdown spectroscopy (LIBS) and extinction spectrum, we obtain sodium atoms with a lifetime of 250 µs. A narrowband tunable continuous wave (CW) 589-nm laser tuned at the D2 line with a modulation frequency around the Larmor frequency is used as the pump beam to polarize sodium atoms in the test magnetic field. We find that the magneto-optical resonance signals vary with different external magnetic fields and the positions of the resonance signal are consistent with the theoretical values. An intrinsic magnetometric sensitivity of 620.4 pT in a 1-Hz bandwidth is achieved.

T-2 toxin induces apoptosis via the Bax-dependent caspase-3 activation in mouse primary Leydig cells.

To explore the toxic effect of T-2 toxin on mouse Leydig cells and its underlying molecular mechanisms, we isolated Leydig cells from mature mice, set-up Leydig cells culture, treated cells with T-2 toxin, evaluated cell proliferation, detected the caspase-3 activity, mitochondrial activity and apoptosis rate, and measured the mRNA levels of Bcl-2, Bax, PARP and caspase-3. T-2 toxin inhibited cell proliferation at concentrations higher than 10-9 M or time more than 12 h, T-2 toxin also decreased Bcl-2 expression at the mRNA levels and mitochondrial activity at concentrations higher than 10-9 M. While, T-2 toxin increased the mRNA expressions of Bax and PARP at concentrations higher than 10-8 M and 10-9 M, respectively, triggered mitochondria-mediated apoptosis, activated downstream caspase-3, and then increased caspase-3 at the activity and mRNA levels at concentrations higher than 10-9 M. These data showed that T-2 toxin appears to activate specific intracellular death-related pathways leading to Bax-dependent caspase-3 activation and the induction of apoptosis in Leydig cells.

Role of luxS in Stress Tolerance and Adhesion Ability in Lactobacillus plantarum KLDS1.0391.

Lactobacillus plantarum, a probiotic, has a high survival rate and high colonization ability in the gastrointestinal tract. Tolerance to the gastrointestinal environment and adhesion to intestinal epithelial cells by some Lactobacillus species (excluding L. plantarum) are related to luxS/AI-2. Here, the role of luxS in tolerance to simulated digestive juice (SDJ) and adhesion to Caco-2 cells by L. plantarum KLDS1.0391 (hereafter, KLDS1.0391) was investigated. The KLDS1.0391 luxS mutant strain was constructed by homologous recombination. When luxS was deleted, acid and bile salt tolerance and survival rates in SDJ significantly decreased (p < 0.05 for all). The ability of the luxS deletion strain to adhere to Caco-2 cells was markedly lower than that of the wild-type strain (p < 0.05). The ability of the luxS mutant strain to adhere (competition, exclusion, and displacement) to Escherichia coli ATCC 25922 was significantly lower than that of the wild-type strain (p < 0.05 for all). A significant decrease was noted only in the exclusion adhesion inhibition of the luxS mutant strain to Salmonella typhimurium ATCC 14028 (p < 0.05). These results indicate that the luxS gene plays an important role in the gastrointestinal environment tolerance and adhesion ability of KLDS1.0391.