Lung stem/progenitor cells are potentially useful for regenerative therapy, for example in repairing damaged or lost lung tissue in patients. Several optical imaging methods and probes have been used to track how stem cells incorporate and regenerate themselves in vivo over time. However, these approaches are limited by photobleaching, toxicity and interference from background tissue autofluorescence. Here we show that fluorescent nanodiamonds, in combination with fluorescence-activated cell sorting, fluorescence lifetime imaging microscopy and immunostaining, can identify transplanted CD45(-)CD54(+)CD157(+) lung stem/progenitor cells in vivo, and track their engraftment and regenerative capabilities with single-cell resolution. Fluorescent nanodiamond labelling did not eliminate the cells' properties of self-renewal and differentiation into type I and type II pneumocytes. Time-gated fluorescence imaging of tissue sections of naphthalene-injured mice indicates that the fluorescent nanodiamond-labelled lung stem/progenitor cells preferentially reside at terminal bronchioles of the lungs for 7 days after intravenous transplantation.

The molecular nature of cancer-associated antigen, CA215 which reacts with RP215 monoclonal antibody and its unique epitope(s)was characterized. RP215 was initially selected and produced from one of 3,000 hybridomas which were generated from mice immunized with the cell extract of OC-3-VGH ovarian cancer cells. This cancer-associated antigen from various sources including cancer cell extract, shed culture medium and affinity-purified forms was analyzed by MALDI-TOF MS (Matrix Adsorption Laser Desorption Ionization-Time of Flight Mass Spectrometry), Western blot, carbohydrate profiling as well as enzyme immunoassays. The results of this study showed that CA215 is homologous to the heavy chains of human immunoglobulins with molecular sizes ranging from 50 to 70 KDa, when probed with RP215 or anti-human immunoglobulin G, A or M. Treatments of cancer cells with NaIO(4) drastically reduce RP215 binding to the carbohydrate-associated epitope(s) of CA215 located on the variable domain of the human immunoglobulin heavy chains. Further studies indicated that CA215 is predominantly expressed by cancer cells in both secreted and membrane-bound monomeric forms. The carbohydrate-associated epitope(s) with pH-sensitive immunoactivity appear to be present only in cancer cell-derived immunoglobulins, but not in normal human immunoglobulins. Compared to normal immunoglobulin G, CA215 contains a significantly higher percentage of N-acetyl and N-glycoyl neuraminic acid (28% vs. 8%) in the O-linked glycans, but a lower content of N-acetylglucosamine (28% vs. 41%) in the N-linked ones. It was concluded from this study that RP215 reacts specifically with carbohydrate-associated epitope(s) of immunoglobulin heavy chains expressed by various human cancer cells.

Background:The Hsp70 chaperone cycle mediates stress-denatured protein refolding. Results: We present the structure of a DnaK-GrpE complex containing the DnaK interdomain linker and substrate-binding domain. Conclusion:Interaction between the DnaK linker/lid regions and the GrpE N-terminal ␣-helix and disordered region are essential for function. Significance: The structure provides a framework for studies concerning interaction of full-length DnaK and GrpE.

The 3-5 microns infrared spectra of the external "Qi" generated by a "Qigong" master from his palm was measured using a III-V compound semiconductor InSb detector. It was found that certain Qigong master can emit two opposite kinds of "Qi": the "facilitating" (beneficial) and "inhibiting" (destroying) "Qi". During the facilitating "Qi" emission, large amount of infrared wave were detected by a temperature rise of the air in the vicinity. When the inhibiting "Qi" was emitted, the infrared wave was absorbed from the environment resulting in a cooling of the air. The temperature rise or drop possibly reflects the fact that the blood flow to the palm was increased or decreased by dilating or constricting the blood vessels through parasympathetic or sympathetic nerves. The biochemical effects of emitted "Qi" from the same Qigong master on the human fibroblast FS-4 were investigated. The facilitating "Qi" caused 1.8% increase of the cell growth in 24 hrs, 10-15% increase of DNA synthesis and 3-5% increase of protein synthesis of the cell in a 2-hr period; while inhibiting "Qi" caused 6% decrease of cell growth in a 24 hr period, 20-23% decrease of DNA synthesis and 35-48% of protein synthesis in a 2-hr period. In addition, we found that the respiration rate of boar sperm increased 12.5-13.0% after receiving 5 min exposure in facilitating "Qi," and a decrease to 45-48% by exposure to 2-min of inhibiting "Qi." The results could be attributed to the effects of emitted "Qi" or energy containing infrared light (wave) and possibly some other types of energy.

The ras oncogene exists in a variety of human cancers, including carcinomas of bladder, breast, colon, kidney, liver, lung, ovary, pancreas, and stomach. The ras genes acquire transforming activity either by enhanced expression or by a single point mutation. A single base-pair mutation at specific sites within ras genes endows them with the capacity to transform certain cell lines in vitro. In this study, we showed the patterns of point mutations in codons 12, 13, and 61 of ras genes in human ovarian cancer. The experimental procedures were isolation of genomic DNA from normal ovary and ovarian cancer tissue specimens, amplification of a genomic DNA segment (about 100 bp) using different 5' and 3' extension primers in the polymerase chain reaction (PCR), labeling and purification of synthetic mutation-specific oligonucleotide probes, slot-blot hybridization, and autoradiography. The three reaction steps for the PCR cycle were: 96 degrees C for 1 min in step 1, 56 degrees C for 1 min in step 2, and 74 degrees C for 1 min in step 3. The PCR reaction was repeated totally for 30 cycles. In 28 tissue specimens of human ovarian cancer examined, one specimen was found with a c-Ha-ras point mutation at codon 12, two had a c-Ki-ras mutation at codon 12, and one had a c-Ki-ras mutation at codon 13.