Deep placement of Mn fertiliser on a sandy soil increased grain yield and reduced split seed in Lupinus angustifolius

Experiments were conducted over two years with Lupinus angustifolius L. on a site with acid sandy soil near Esperance, Western Australia to determine if deep placed manganese fertilizer increases lupin grain yield. Manganese at 4 and 8 kg ha⁻¹ was placed below the surface immediately before sowing at 4, 20 and 30 cm and 4, 8, 12, 16 and 20 cm in 1987 and 1988 respectively. Foliar Mn applied at 1 kg ha⁻¹ when the first order laterals were in mid-flowering stage, was also compared. Increasing the depth of Mn placement increased grain yield in both years. The deepest placed Mn increased grain yields by 255 kg ha⁻¹ (10%) and 430 kg ha⁻¹ (106%) in year 1 and year 2 over the shallow (4 cm) placed Mn. The higher responses to deep placed Mn occurred in year 2, the year with the driest spring and most intense aphid infestations. Foliar applied Mn was as effective as most deep placed Mn treatments, except for the highest rate (8 kg ha⁻¹) at the greatest depth (20 cm) in year 2. The higher rate of applied Mn gave the best grain yields. This revised version was published online in June 2006 with corrections to the Cover Date.     

Comparative Study of Glial Marker Proteins in the Hypoplastic Cerebellum of Jaundiced Gunn Rats

The behavior of marker proteins of glial cells [alpha-enolase, beta-S100 protein, and glial fibrillary acidic protein (GFAP)] was investigated quantitatively by using enzyme immunoassay systems during the development of cerebellar hypoplasia in jaundiced Gunn rats. A neuronal marker protein, gamma-enolase, was also measured as a reference. At postnatal day 8 corresponding to the early stage of cerebellar damage, the amount of beta-S100 on a protein basis was significantly higher in jaundiced homozygotes (jj) than in control nonjaundiced heterozygotes (j+), whereas no differences in alpha- and gamma-enolases and GFAP were observed between the two groups of rats. At days 15 and 30, which correspond, respectively, to the advanced and late stages of cerebellar damage, the three glial proteins, especially GFAP, were higher and the neuronal protein was lower in the jj rat cerebellum than in the control. These results are consistent with the reported histological observations that neuronal cells are vulnerable and damaged by bilirubin, whereas glial cells seem to be less sensitive. On the other hand, the amounts of beta-S100 and alpha-enolase per cerebellum were significantly lower in jj rats at days 15 and 30, as in the case of gamma-enolase, whereas that of GFAP remained at the same level as the control at day 15 and showed a slight but significant decrease at day 30. The possibility is suggested that beta-S100 and GFAP may be available as biochemical indicators of glial cells, especially in the early and advanced stages of cerebellar damage, respectively, but that alpha-enolase is less available.     

Acidic stress promotes a glioma stem cell phenotype

Malignant gliomas are lethal cancers that display cellular hierarchies with cancer stem cells at the apex. Glioma stem cells (GSCs) are not uniformly distributed, but rather located in specialized niches, suggesting that the cancer stem cell phenotype is regulated by the tumor microenvironment. Indeed, recent studies show that hypoxia and its molecular responses regulate cancer stem cell maintenance. We now demonstrate that acidic conditions, independent of restricted oxygen, promote the expression of GSC markers, self-renewal and tumor growth. GSCs exert paracrine effects on tumor growth through elaboration of angiogenic factors, and low pH conditions augment this expression associated with induction of hypoxia inducible factor 2α (HIF2α), a GSC-specific regulator. Induction of HIF2α and other GSC markers by acidic stress can be reverted by elevating pH in vitro, suggesting that raising intratumoral pH may be beneficial for targeting the GSC phenotype. Together, our results suggest that exposure to low pH promotes malignancy through the induction of a cancer stem cell phenotype, and that culturing cancer cells at lower pH reflective of endogenous tumor conditions may better retain the cellular heterogeneity found in tumors.     

Enhanced Glial Fibrillary Acidic Protein RNA Response to Fornix Transection in Aged Mice

Abstract: The effects of age on basal and lesion-induced changes in astrocyte RNA messages reported to respond to neurodegeneration were examined in the mouse brain. The first study found an age-related increase in glial fibrillary acidic protein RNA throughout the brain. Other astrocyte RNAs remained generally stable with age. We hypothesize this increase is due to astrocytes undergoing a mild reaction to the small amount of synaptic degeneration occurring with usual aging. To test this theory, we used an experimental model of modest synaptic loss in the hippocampus by transecting the fimbria/fornix bundle in mice and examined the same series of messages. In situ hybridization revealed the expected increase in glial fibrillary acidic protein RNA after the lesion; however, we unexpectedly found that aged mice showed a greater magnitude of this response, which appeared to develop more slowly. There was no significant change in the hippocampus for any of the other messages, although responses were observed at the site of transection. This study supports the idea that the age-related increase in glial fibrillary acidic protein may be secondary to modest synaptic degeneration. We also demonstrated an exaggerated reactive astrocytic response in aged mice, which may be associated with age-related deficits in reactive synaptogenesis and behavioral recovery in normal aging.     

High expression of GLT-1 in hippocampal CA3 and dentate gyrus subfields contributes to their inherent resistance to ischemia in rats

It is well known that neurons in the CA3 and dentate gyrus (DG) subfields of the hippocampus are resistant to short period of ischemia which is usually lethal to pyramidal neurons in hippocampal CA1 subfield. The present study was undertaken to clarify whether the inherent higher resistance of neurons in CA3 and DG to ischemia is associated with glial glutamate transporter-1 (GLT-1) in rats. Western blot analysis and immunohistochemistry assay showed that the basal expressions of GLT-1 in both CA3 and DG were much higher than that in CA1 subfield. Mild global brain ischemia for 8 min induced delayed death of almost all CA1 pyramidal neurons and marked GLT-1 down-regulation in the CA1 subfield, but it was not lethal to the neurons in either CA3 or DG and induced GLT-1 up-regulation and astrocyte activation showed normal soma and aplenty slender processes in the both areas. When the global brain ischemia was prolonged to 25 min, neuronal death was clearly observed in CA3 and DG accompanied with down-regulation of GLT-1 expression and abnormal astrocytes represented with hypertrophic somas, but shortened processes. After down-regulating of GLT-1 expression and function by its antisense oligodeoxynucleotides or inhibiting GLT-1 function by dihydrokainate, an inhibitor of GLT-1, the mild global brain ischemia for 8 min, which usually was not lethal to CA3 and DG neurons, induced the neuronal death in CA3 and DG subfields. Taken together, the higher expression of GLT-1 in the CA3 and DG contributes to their inherent resistance to ischemia.     

Fibronectin associated with the glial component of embryonic brain cell cultures

In a basic approach to investigations of neuronal–glial interactions during both normal brain development and its pathogenesis, embryonic brain cell populations were fractionated into purified neuronal and glial components. Using separation procedures based on differential adhesion and cytotoxicity, the isolated neuronal and glial phenotypes could be identified by distinct morphological and biochemical characteristics, including the visualization of glial fibrillary acid protein (GFA) within glial cells in immunohistochemical assays with monospecific anti-GFA serum. When unfractionated cerebrum cells dissociated from 10-day chick or 14-day mouse embryos were plated as monolayers and cultured for 1-14 days, monospecific antiserum against fibronectin (LETS glycoprotein) was found to react with many, but not all, of the cells as revealed by indirect immunofluorescence microscopy. The isolated neuronal and glial components of these populations were used to determine whether the appearance of membrane-associated fibronectin was characteristic of one cell type or the other, or both, and if neuronal–glial cell interaction was required for its expression. It was found that the surfaces of glial cells, completely isolated from neurons, showed an intense fluorescent reaction to the anti-fibronectin serum. In contrast, the purified neuronal cultures showed no fluorescence with either the anti-GFA or anti-fibronectin sera. These results demonstrate fibronectin as a cell surface protein associated primarily with glial cells and independent of neuronal–glial cell interaction for its expression. Furthermore, the results indicate that the fibronectin observed on glial cell surfaces in these cultures is produced endogenously and is not due to the preferential binding of fibronectin present in the culture medium. The role of fibronectin as an adhesive molecule in neuronal–glial interactions is discussed.     

Glial precursor cell transplantation therapy for neurotrauma and multiple sclerosis

Traumatic injury to the brain or spinal cord and multiple sclerosis (MS) share a common pathophysiology with regard to axonal demyelination. Despite advances in central nervous system (CNS) repair in experimental animal models, adequate functional recovery has yet to be achieved in patients in response to any of the current strategies. Functional recovery is dependent, in large part, upon remyelination of spared or regenerating axons. The mammalian CNS maintains an endogenous reservoir of glial precursor cells (GPCs), capable of generating new oligodendrocytes and astrocytes. These GPCs are upregulated following traumatic or demyelinating lesions, followed by their differentiation into oligodendrocytes. However, this innate response does not adequately promote remyelination. As a result, researchers have been focusing their efforts on harvesting, culturing, characterizing, and transplanting GPCs into injured regions of the adult mammalian CNS in a variety of animal models of CNS trauma or demyelinating disease. The technical and logistic considerations for transplanting GPCs are extensive and crucial for optimizing and maintaining cell survival before and after transplantation, promoting myelination, and tracking the fate of transplanted cells. This is especially true in trials of GPC transplantation in combination with other strategies such as neutralization of inhibitors to axonal regeneration or remyelination. Overall, such studies improve our understanding and approach to developing clinically relevant therapies for axonal remyelination following traumatic brain injury (TBI) or spinal cord injury (SCI) and demyelinating diseases such as MS.     

Recovery of Methanogenesis Following Summer Drought in Soils from Two Cool Temperate Peatlands,New York State,USA

Following a summer drought, intact cores of peat soil from two cool temperate peatlands (a rain-fed bog and a groundwater-fed swamp) were exposed experimentally to three different water table levels. The goal was to examine recovery of anaerobic methanogenesis and to evaluate peat soil decomposition to methane (CH₄), carbon dioxide (CO₂), and dissolved organic carbon (DOC) upon rewetting. Methane emission from soils to the atmosphere was greatest (mean = 80 μmol m^?2 s^?1) when the entire peat core was rewetted quickly; emission was negligible at low water level and when peat cores were rewetted gradually. Rates of CO₂ emission (mean = 1.0 μmol m^?2 s^?1) were relatively insensitive to water level. Concentrations of CH₄ in soil air spaces suggest that onset of methanogenesis induces, but later represses, aerobic oxidation of CH₄ above the water table. Concentrations of CO₂ suggest production at the soil surface of swamp peat versus at greater depths in bog peat. Portions of peat soil incubated in vitro without oxygen (O₂) exhibited a lag before the onset of methanogenesis, and the lag time was less in peat from the cores rewetted quickly. The inhibition of methanogenesis by the selective inhibitor 2-bromoethanesulfonic acid (BES) decreased CO₂ production by 20 to 30% but resulted in an increase in concentrations of DOC by 2 to 5 times. The results show that methanogens in peat soils tolerate moderate drought, and recovery varies among different peat types. In peat soils, the inhibition of methanogenesis might enhance DOC availability.     

黑曲霉固态发酵生产酸性β-甘露聚糖酶

以黑曲霉WA301为生产菌固态发酵生产酸性β－甘露聚糖酶,较适的培养基组成和培养条件为：麸皮10g,魔芋粉0.4g,豆饼粉1.5g,硫酸铵0.2g,起始湿度55％,pH自然,发酵温度35℃,发酵周期约96h。在此条件下,WA301的酸性β－甘露聚糖酶产率为950U／g干曲左右。