Transgenic mouse lines were generated that express the Cre recombinase under the control of the distal promoter of the mouse Lck gene. Cre recombination in four of these lines of transgenic mice was characterized at the single cell level using ROSA26-regulated loxP-Stop-loxP-βgeo and loxP-Stop-loxP-YFP reporter mouse lines. Two of the lines showed T cell-restricted Cre recombination, whereas the other two also expressed Cre in B cells, NK cells, and monocytes. Cre recombination began at a late stage of T cell development (at or after up-regulation of the TCR during positive selection) in the two T cell-restricted lines. Lines of mice that express the Cre recombinase at late stages of thymocyte development are of value for determining the impact of mutations on T cell function in the absence of complicating effects on early thymocyte selection.
Aging is the greatest risk factor for most neurodegenerative diseases, which is associated with decreasing cognitive function and significantly affecting life quality in the elderly. Computational analysis suggested that 4 anthocyanins from chokeberry fruit increased Klotho (aging-suppressor) structural stability, so we hypothesized that chokeberry anthocyanins could antiaging. To explore the effects of anthocyanins treatment on brain aging, mice treated with 15 or 30 mg/kg anthocyanins by gavage and injected D-galactose accelerated aging per day. After 8 weeks, cognitive and noncognitive components of behavior were determined. Our studies showed that anthocyanins blocked age-associated cognitive decline and response capacity in senescence accelerated mice. Furthermore, mice treated with anthocyanins-supplemented showed better balance of redox systems (SOD, GSH-PX, and MDA) in all age tests. Three major monoamines were norepinephrine, dopamine, and 5-hydroxytryptamine, and their levels were significantly increased; the levels of inflammatory cytokines (COX2, TGF-β1, and IL-1) transcription and DNA damage were decreased significantly in brains of anthocyanins treated mice compared to aged models. The DNA damage signaling pathway was also regulated with anthocyanins. Our results suggested that anthocyanins was a potential approach for maintaining thinking and memory in aging mice, possibly by regulating the balance of redox system and reducing inflammation accumulation, and the most important factor was inhibiting DNA damage.
Exposure of isolated photosystem I (PSI) complexes to illumination (2300 μE m−2 s−1) for various periods of time resulted in striking changes in their absorption spectra. A 6 nm blueshift of the absorption maximum in the red was detected after 100 min illumination. The fourth derivative of the absorption spectra verifies that the main change of the red peak was attributed to the 682 nm absorption band. Further, it was also shown that a shoulder in the absorption spectra located around 470 nm decreased after the first 5 min of illumination and almost disappeared after 40 min illumination, suggesting that chlorophyll b bound to light‐harvesting complex I (LHCI) is also sensitive to excess light. A maximum inhibitory effect on the oxygen uptake rates and a strong stimulation were observed when the PSI complexes were exposed to illumination for about 20 and 40 min, respectively. Sodium dodecyl sulfate‐polyacrylamide gel electrophoresis shows that LHCI‐680 started to degrade during the first 5 min of illumination and almost completely disappeared after 40 min of illumination. These observations demonstrated that LHCI was more sensitive to illumination than the PsaA/B subunits which also presented some degradation signs after 40 min illumination. In addition, insoluble–cohesive‐denatured proteins also appeared between the stacking and resolving gel after prolonged illumination (100 min). A photoprotective function of LHCI for the PSI reaction center is proposed.
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