Precise intensity correlation measurement for atomic resonance fluorescence from optical molasses.

We measured the intensity correlation of true thermal light scattered from cold atoms in an optical molasses. Using a single-mode fiber as a transverse mode filter, measurement with maximally high spatial coherence was realized, allowing us to observe ideal photon bunching with unprecedented precision. The measured intensity correlation functions showed a definite bimodal structure with fast damped oscillation from the maximum value of 2.02(3) and slow monotonic decay toward unity. The oscillation can be understood as an interference between elastic and inelastic scattering fields in resonance fluorescence.

Induction of tumor-specific cytotoxicity and apoptosis by doxorubicin.

Doxorubicin (adriamycin), an anthracycline antibiotic, showed higher cytotoxic activity against human tumor cell lines (oral squamous cell carcinoma HSC-2, HSC-3, submandibular gland carcinoma HSG, promyelocytic leukemia HL-60) than against normal human cells (gingival fibroblast HGF, pulp cell HPC, periodontal ligament fibroblast HPLF). Doxorubicin activated caspases 3, 8 and 9 in both HSC-2 and HL-60 cells, but induced internucleosomal DNA fragmentation only in HL-60 cells. Western blot analysis showed that doxorubicin did not significantly change the intracellular concentration of Bcl-2, Bax and Bad in HL-60 cells. Real-time PCR analysis showed that HPC cells expressed the highest amount of mdr1 mRNA, followed by HSC-2 > HGF > HSC-3 > HPLF > HSG > HL-60. ESR spectroscopy showed that doxorubicin produced no discernible radical under alkaline conditions (pH 7.4 to 10.5) except at pH 12.5, and it did not scavenge O2-, NO and DPPH radicals. The present study demonstrates that doxorubicin induces the tumor-specific cytotoxicity and some, but not all, apoptosis markers possibly by a radical-independent mechanism, and that mdr1 expression in the tumor cells is not related to the tumor specificity of doxorubicin.

Cytotoxicity and radical modulating activity of Moxa smoke.

The biological activities of Moxa, used as moxibustion, have not been well documented. We investigated here Moxa smoke for its tumor-specific cytotoxicity, anti-HIV activity, radical intensity and radical scavenging activity, in comparison with previously published data of Moxa extract. Moxa smoke showed slightly higher cytotoxicity against human tumor cell lines (oral squamous cell carcinoma HSC-2, HSC-3, promyelocytic leukemia HL-60) than against normal oral cells (gingival fibroblast HGF, pulp cell HPC, periodontal ligament fibroblast HPLF), yielding a tumor specificity index of 1.29. Moxa smoke dose-dependently induced internucleosomal DNA fragmentation, activation of caspases 3, 8 and 9, and slightly modified the expression of apoptosis-related proteins (Bcl-2, Bad, Bax) in HL-60 cells, but to much lesser extents than attained by positive controls (UV irradiation, actinomycin D treatment). ESR spectroscopy showed that Moxa smoke generated semiquinone-type radicals under alkaline conditions, and scavenged O2(-), hydroxyl radical, singlet oxygen and NO. All Moxa smoke preparations showed no apparent anti-HIV activity. These data demonstrate the antitumor potential of Moxa smoke.

Inhibition by Moxa smoke of NO production and iNOS expression in mouse macrophage-like cells Raw 264.7.

The biological activities of Moxa, used as moxibustion, have not been well documented. We investigated the effect of Moxa smoke on nitric oxide (NO) production by mouse macrophage-like Raw 264.7 cells. Moxa smoke failed to stimulate the Raw 264.7 cells to produce detectable amounts of NO, but rather inhibited the NO production by lipopolysaccharide (LPS)-activated Raw 264.7 cells. The 50% inhibitory concentration (IC50) of NO production by Moxa smoke (0.16%) was one order lower than the 50% cytotoxic concentration (CC50) (4.67%). Western blot and RT-PCR analyses demonstrated that a slightly higher concentration of Moxa is required to reduce the iNOS expression at protein and mRNA levels (IC50 = 0.99 and 2.03%, respectively). The inhibition of NO production by Moxa smoke is, thus, probably due to both the inhibition of iNOS expression and radical-scavenging activity. The present data suggest the possible anti-inflammatory effect of Moxa smoke.