Pathogenicity of Spiroplasma taiwanense for larval Aedes aegypti mosquitoes

Helical replicative forms, but not the persistent non-replicative forms, of Spiroplasma taiwanense Abalain-Colloc et al. (isolated from the mosquito Anopheles sinensis Wiedemann in Taiwan) were shown to reduce significantly the survival of Aedes aegypti (L.) mosquito larvae reared in 10 ml of water with 0.3 ml of S.taiwanense suspensions added on days 0 and 3. The suspensions contained, respectively, helical forms at a concentration of 10(9) Colour Change Units (CCU)/ml and persistent forms at 10(6) CCU/ml. It is suggested that S.taiwanense, or toxins produced from it, are potentially useful for use in integrated mosquito control programmes.     

Effects of Calphostin C,Specific PKC Inhibitor on TPA-Induced Normal Human Melanocyte Growth,Morphology and Adhesion

Normal human melanocytes, which rarely undergo mitosis in vivo, require many growth factors and growth-stimulating agents in vitro, such as basic fibroblast growth factor (bFGF) and cyclic adenosine monophosphate-stimulating agents or 12-0-tetrade-canoylphorbol 13-acetate (TPA), to proliferate. TPA, known as a protein kinase C (PKC)-activator, supports normal human melanocyte growth and influences on melanocyte dendrite formation. We have further confirmed the role of the PKC-mediated pathway in the TPA-dependent melanocyte functions—i.e., proliferation, morphology, and adhesion—using Calphostin C (CPC), a highly specific PKC inhibitor. Melanocytes require the continual presence of TPA for growth in culture. Addition of 8 nM TPA to the medium increased melanocyte growth by 198.4 ± 2.3% of that without TPA. The growth induction by TPA was suppressed by the addition of 10 nM CPC at the level comparable to that without TPA without any morphological alterations. Significant levels of PKC were detected in melanocytes chronically exposed to TPA as determined by Western blotting. A long-term exposure to TPA (more than 5 days) resulted in marked reduction of melanocyte adhesion to plastic cell culture dishes, both uncoated and coated with type IV collagen. By the addition of 10 nM CPC in the adhesion assay, the melanocyte adhesion was further inhibited in both conditions. These results indicated the critical involvement of PKC activation in the TPA-dependent melanocyte functions. Continuous activation of PKC by TPA is implicated in melanocyte growth stimulation. TPA also has effects on melanocyte morphology, causing the formation of long extended dendrites with little cytoplasm. However, inhibition of PKC activation by CPC does not affect the melanocyte morphology, and CPC reduces melanocyte adhesion to uncoated or type IV collagen coated plastic cell culture dishes.     

Degradation of pectic substances in green flax fibre by Erwinia carotovora

In this paper, we report that Erwinia carotovora can perform controlled biological pectinolysis of green flax fibre. The degradation of pectic substances is considered a key step during this process and is estimated by determining the cation exchange capacity (CEC). A CEC characteristic of a ‘good retting degree’, is reached after 20 h incubation, whatever the tested temperature and initial pectate lyase activity of the bacterial culture. Similar results are obtained after only 4 h, at a temperature of 45°C and the pectate lyase activity is greater than 2 nmol ml^-1 min^-1. The linear relationship between the CEC and the weight loss of green fibre which is established, allows us to estimate an equivalent weight of 1000 g eq^-1 for the solubilised polymers.     

Ca2+ and UVB Radiation Have No Effect on E-Cadherin-Mediated Melanocyte-Keratinocyte Adhesion

Direct cell-cell contact between melanocytes and keratinocytes has been shown to play an important role in the regulation of human melanocyte function and skin pigmentation. An important role for the calcium-dependent epithelium-specific cell adhesion molecule, E-cadherin, in melanocyte-keratinocyte adhesion was suggested previously. To further clarify regulation of E-cadherin-mediated melanocyte-keratinocyte interactions, we investigated the effects of physiological (Ca²⁺) and environmental (ultraviolet B [UVB] radiation) stimuli on the expression and functional activity of E-cadherin in melanocyte-keratinocyte adhesion. Expression of E-cadherin mRNA was detected by Northern blot analysis in cultured normal human melanocytes at levels similar to those in keratinocytes. Flow cytometry analysis with anti-human and anti-mouse-E-cadherin antibodies (anti-uvomorulin and ECCD-2) showed that cultured normal human keratinocytes, melanocytes, and two metastatic melanoma cell lines express E-cadherin strongly on the cell surfaces. Melanocyte adhesion, particularly to differentiating keratinocytes (cultured in 1.2 mM calcium) but not to proliferating keratinocytes or to fibroblasts, was decreased by 41.7 ± 4.5% in the absence of 1 mM Ca²⁺ during the binding assay. Addition of anti-mouse-E-cadherin antibody (ECCD-1) to the binding assay inhibited the adhesion of melanocytes to differentiating keratinocytes by 88.2 ± 1.1%, while addition of anti-P-cadherin antibody (PCD-1) had no effect. The levels of E-cadherin expression in melanocytes were not changed by the presence of calcium (1 mM) in the medium or by UVB irradiation (20 mJ/cm²) for one day before flow cytometry analysis. Moreover, these treatments had no effect on melanocyte-keratinocyte adhesion. These results demonstrate that E-cadherin is strongly involved in melanocyte adhesion to keratinocytes and suggest the implication of E-cadherin in the overall regulation of the skin pigmentary system.