Differences in absorption and/or scattering of cancerous and normal skin have the potential to provide a basis for noninvasive cancer detection. In this study, we have determined and compared the in vitro optical properties of human epidermis, dermis, and subcutaneous fat with those of nonmelanoma skin cancers in the spectral range from 370 to 1600 nm. Fresh specimens of normal and cancerous human skin were obtained from surgeries. The samples were rinsed in saline solution and sectioned. Diffuse reflectance and total transmittance were measured using an integrating sphere spectrophotometer. Absorption and reduced scattering coefficients were calculated from the measured quantities using an inverse Monte Carlo technique. The differences between optical properties of each normal tissue-cancer pair were statistically analyzed. The results indicate that there are significant differences in the scattering of cancerous and healthy tissues in the spectral range from 1050 to 1400 nm. In this spectral region, the scattering of cancerous lesions is consistently lower than that of normal tissues, whereas absorption does not differ significantly, with the exception of nodular basal cell carcinomas (BCC). Nodular BCCs exhibit significantly lower absorption as compared to normal skin. Therefore, the spectral range between 1050 and 1400 nm appears to be optimal for nonmelanoma skin cancer detection.

In the developing retina, the microvessels form by differentiation of endothelial precursor cells in a process referred to as vasculogenesis. Experiments using in vivo and in vitro model systems were designed to determine the specific influence of astrocytes on this process. Immunolocalization analyses of retinal vasculogenesis in vivo showed that astrocytes spread within the nerve fiber layer of the neonatal rat retina just ahead of the forming vessels. Then, endothelial precursor cells align themselves in register with the astrocytes. In contact with astrocytes, precursor cells differentiate as vascular endothelium, as indicated by lumen formation and patency to red blood cells. Experiments in vitro using cell culture and conditioned medium approaches showed that cell-cell contact between rat brain astrocytes and bovine retinal endothelial cells results in release of soluble factors, inhibiting endothelial cell growth and inducing morphological differentiation in capillary-like structures. Thus, it is suggested that astrocytes lay down the pattern for vasculogenesis and induce the elongation and alignment of endothelial precursor cells into a prevascular meshwork. In contact with astrocytes, precursor cells differentiate as vascular endothelium. Furthermore, this cell-cell contact with astrocytes apparently inhibits endothelial cell growth and stimulates their elongation, alignment, and morphogenic differentiation by means of the release or activation of soluble, growth factor-like substances.

Objective: Serum and synovial fluid (SF) chemokine ligand 2 (CCL2)/monocyte chemoattractant protein 1 (MCP-1) concentrations have been identified to be increased in osteoarthritis (OA) patients. The scope of this study was to examine CCL2 concentrations in serum and SF of knee OA patients and to explore their association with patientreported symptomatic severity. Method: One hundred and sixty-one knee OA patients and 138 healthy controls were enrolled into the study from our hospital. We collected Western Ontario and McMaster Universities Arthritis Index (WOMAC) scores from OA patients and measured CCL2 concentrations in serum and SF using enzyme-linked immunosorbent assay method, and correlation between WOMAC scores and CCL2 concentrations were analysed. Results: CCL2 concentrations in SF instead of serum were independently and positively associated with self-reported greater pain (r ¼ 0.460, P < 0.001) and physical disability (r ¼ 0.561, P < 0.001) in OA patients. Conclusion: CCL2 in SF might serve as a novel and reliable biomarker for assessing symptomatic severity of OA.

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