Effect of rootzone construction on soil physical properties and playing quality of golf greens under New Zealand conditions : a thesis presented in partial fulfilment of the requirements for the degree of Master of Applied Science in Plant Science at Massey University

A field experiment was designed to examine the effect of five different rootzone constructions (partially amended sand, silt soil, pure sand, fully amended sand and partially amended plus zeolite sand) and aeration methods (untreated control, HydroJect, Verti-drain and scarifying) on soil physical properties, root development and playing quality of golf greens. The five rootzone constructions were randomly arranged in three blocks. A split plot design was superimposed on the rootzone constructions using different aeration methods. Aeration treatments were carried out in the spring and autumn of 1998. Measurements of bulk density, total porosity, volumetric moisture content, air-filled porosity, infiltration rate, oxygen diffusion rate, saturated hydraulic conductivity, root mass, organic matter content, surface hardness and green speed were made to monitor differences between treatments. This study found there was no benefit of fully amended sand rootzone compared with partially amended sand rootzones (either plus or without zeolite). Although root development was greater in the pure sand rootzone, this occurred predominantly in the top 50 mm. Excessive accumulation near the surface of the profile can have detrimental impacts on turf growth. Rootzone construction had an important effect on surface hardness, i.e. pure sand rootzone produced the hardest surface, silt soil rootzone the softest and amended sand rootzones intermediate hardness. Rootzone construction had no effect on green speed in this study. Aeration treatment had no effect on any of the soil, plant or playing quality parameters measured in this study. This suggests either aeration treatments were very short lived or that long term effects of aeration treatments were not yet apparent

Tetramethylpyrazine protects Schwann cells from ischemia-like injury and increases cell survival in cold ischemic rat nerves

Tetrametilpirazina (TMP), o principal componente do extrato de Ligusticum wallichi Franchat (erva chinesa), apresenta propriedades neuroprotetoras na isquemia. Nesse estudo, avaliamos seus efeitos protetores nas células de Schwann (SC), cultivando-as na presença de condições de depleção de oxigênio da glicose (OGD) e medindo a sobrevivência dos nervos de ratos isquêmicos pelo resfriamento. No modelo de lesão isquêmica em SC induzida por OGD, demonstramos que o tratamento com TMP não somente reduziu as perdas de viabilidade celular induzida por OGD, a morte celular, a apoptose de SC dose-dependente e inibiu a liberação de LDH, mas, também, suprimiu a infra-regulação do Vcl-2 e a supra-regulação de Bax e caspase-3, e inibiu a consequente ativação da caspase-3. No modelo de nervo isquêmico por resfriamento, observamos que a exposição prolongada ao resfriamento por quatro semanas estava, marcadamente, associada com a ausência de SC, com o decréscimo da viabilidade celular e a apoptose em segmentos de nervo incubados na solução da Universidade de Wisconsin apenas. Entretanto, a TMP atenuou o dano no segmento do nervo preservando SC e antagonizando a diminuição da viabilidade da fibra nervosa e o aumento das células TUNEL-positiva de modo dose-dependente. De forma conjunta, nossos resultados indicam que o TMP não só fornece efeitos protetores em um modelo de dano semelhante à isquemia de SC de ratos cultivados pela regulação de BCl-2, Bax e caspase 3, mas, também, aumenta a sobrevivência celular e suprime a apoptose no modelo de isquemia por resfriamento por exposição prolongada por quatro semanas. Então, TMP pode ser uma estratégia terapêutica eficaz para prevenir doenças isquêmicas do sistema nervoso periférico e melhora a armazenagem do nervo periférico.Tetramethylpyrazine (TMP), a major active ingredient of Ligusticum wallichi Franchat extract (a Chinese herb), exhibits neuroprotective properties in ischemia. In this study, we assessed its protective effects on Schwann cells (SCs) by culturing them in the presence of oxygen glucose deprivation (OGD) conditions and measuring cell survival in cold ischemic rat nerves. In the OGD-induced ischemic injury model of SCs, we demonstrated that TMP treatment not only reduced OGD-induced cell viability losses, cell death, and apoptosis of SCs in a dose-dependent manner, and inhibited LDH release, but also suppressed OGD-induced downregulation of Bcl-2 and upregulation of Bax and caspase-3, as well as inhibited the consequent activation of caspase-3. In the cold ischemic nerve model, we found that prolonged cold ischemic exposure for four weeks was markedly associated with the absence of SCs, a decrease in cell viability, and apoptosis in preserved nerve segments incubated in University of Wisconsin solution (UWS) alone. However, TMP attenuated nerve segment damage by preserving SCs and antagonizing the decrease in nerve fiber viability and increase in TUNEL-positive cells in a dose-dependent manner. Collectively, our results indicate that TMP not only provides protective effects in an ischemia-like injury model of cultured rat SCs by regulating Bcl-2, Bax, and caspase-3, but also increases cell survival and suppresses apoptosis in the cold ischemic nerve model after prolonged ischemic exposure for four weeks. Therefore, TMP may be a novel and effective therapeutic strategy for preventing peripheral nervous system ischemic diseases and improving peripheral nerve storage