Interaction between the extracellular matrix and lymphatics: Consequences for lymphangiogenesis and lymphatic function

The lymphatic system is important for body fluid balance as well as immunological surveillance. Due to the identification of new molecular markers during the last decade, there has been a recent dramatic increase in our knowledge on the molecular mechanisms involved in lymphatic vessel growth (lymphangiogenesis) and lymphatic function. Here we review data showing that although it is often overlooked, the extracellular matrix plays an important role in the generation of new lymphatic vessels as a response to physiological and pathological stimuli. Extracellular matrix-lymphatic interactions as well as biophysical characteristics of the stroma have consequences for tumor formation, growth and metastasis. During the recent years, anti-lymphangiogenesis has emerged as an additional therapeutic modality to the clinically applied anti-angiogenesis strategy. Oppositely, enhancement of lymphangiogenesis in situations of lymph accumulation is seen as a promising strategy to a set of conditions where few therapeutic avenues are available. Knowledge on the interaction between the extracellular matrix and the lymphatics may enhance our understanding of the underlying mechanisms and may ultimately lead to better therapies for conditions where reduced or increased lymphatic function is the therapeutic target.     

Effect of thiram on plant growth and rhizosphere microflora of barley and nodulation in cowpea

Summary Thiram applied as a seed dresser fungicide had no inhibitory effect on seedling height and rhizosphere microflora of barley plants (Hordeum vulgare) and on nodulation of cowpea plants (Vigna catjang).     

Dose and duration related methylmercury deposition, glycosidases inhibition, myelin degeneration and chelation therapy

Methylmercury accumulation in different parts of the CNS (olfactory bulbs, cerebral hemispheres, cerebellum, medulla oblongata and spinal cord) in relation to the cytoarchitectural changes in myelin sheath as well as in glycosidases levels have been reported. Male albino rats were treated with low and high doses of methylmercury chloride (1 mg/kg and 10 mg/kg) N-acetyl-DL-homocysteine thiolactone (40 mg/kg and 80 mg/kg) and glutathione (100 mg/kg and 150 mg/kg) for varied time periods. The study shows a dose and duration dependent accumulation of mercury in all the CNS areas coinciding with a progressive myelin degeneration and inhibition of the glycosidases. A casual relationship between the amount of mercury accumulation and the extent of enzymes inhibition, in any particular area of CNS, could not be established. Similarly none of the antagonists is (though has been successful in recovering the enzymes and lessening the mercury burden in a few isolated cases) able to bring an absolute control value in any group.