Does (K+Mg+Ca+P) fertilization lead to recovery of tree health in a nitrogen stressed Quercus rubra L. stand?

In The Netherlands atmospheric deposition of nitrogen compounds to forest ecosystems has been very high for some decades and has led to severe nutritional imbalances in soils as well as in trees. At this moment legislation is not fully in effect with respect to lowering emission/deposition fluxes, particularly of nitrogen. The trees suffer mainly from severe magnesium, potassium and calcium and sometimes phosphorus deficiencies. In this study it was investigated whether fertilization with potassium, magnesium, calcium and phosphorus could prevent a Quercus rubra stand from further decline by restoring the nutritional balance, though the detrimental input of nitrogen compounds still continues. Three fertilization treatments were applied: (i) a standard dose of 1250 kg.ha(-1) containing 60 kg P.ha(-1) (as P2O5), 100 kg K.ha(-1) (as K2O), 80 kg Mg.ha(-1) (as MgO) and 340 kg Ca.ha(-1) (as CaCO3); (ii) two times the standard dose; and (iii) three times the standard dose. Soil solution chemistry showed that the highest dose led to the most significant results: an improved nutrient balance and an increased availability of nutrients. After one growing season following fertilization, the trees looked much healthier and crown density had increased. This revitalization lasted for at least four years. For tree health the mid dose seemed appropriate. After the first growing season potassium is the most mobile nutrient, in the soil and also in the trees, but tended to decrease in the fourth year after fertilization. Magnesium and calcium reached normal values in the leaves after four growing seasons. No obvious effects of phosphorus were found.     

Two unbalanced segregation products due to a maternal t(7;16)inv(16)

We report a prenatal case of a maternally inherited abnormal chromosome 16, originally interpreted as a pericentric inversion only, but after family studies re-interpreted as a pericentric inversion (16) accompanied by an unbalanced (7;16) translocation. Because of the inversion 16 and an elder son with developmental delay and craniofacial dysmorphic features, in the past karyotyped as 46,XY, the chromosomes 16 of the mother and son were carefully re-examined. Using a whole chromosome 16 paint and sub-telomere probes of 16p and 16q, the karyotype of the mother was shown to be 46,XX,inv(16)(p11.2q23.2).ish t(7;16)(q36;p13.3)inv(16). Subsequently one chromosome 16 of the elder son appeared to be a der(16)t(7;16)(q36;p13.3). This is probably the result of a meiotic crossover between the chromosomes 16 in the mother. The prenatal karyotype was finally interpreted as 46,XY,inv(16)(p11.2q23.2).ish der(16)t(7;16)(q36;p13.3)inv(16). This is the same cytogenetic imbalance as his elder brother: a partial trisomy of chromosome 7 (q36→qter) and a partial monosomy of chromosome 16 (p13.3→pter). Copyright © 2001 John Wiley & Sons, Ltd.