Effects of competition and herbivory over woody seedling growth in a temperate woodland trump the effects of elevated CO2.

A trend of increasing woody plant density, or woody thickening, has been observed across grassland and woodland ecosystems globally. It has been proposed that increasing atmospheric [CO2] is a major driver of broad scale woody thickening, though few field-based experiments have tested this hypothesis. Our study utilises a Free Air CO2 Enrichment experiment to examine the effect of elevated [CO2] (eCO2) on three mechanisms that can cause woody thickening, namely (i) woody plant recruitment, (ii) seedling growth, and (iii) post-disturbance resprouting. The study took place in a eucalypt-dominated temperate grassy woodland. Annual assessments show that juvenile woody plant recruitment occurred over the first 3 years of CO2 fumigation, though eCO2 did not affect rates of recruitment. Manipulative experiments were established to examine the effect of eCO2 on above-ground seedling growth using transplanted Eucalyptus tereticornis (Myrtaceae) and Hakea sericea (Proteaceae) seedlings. There was no positive effect of eCO2 on biomass of either species following 12 months of exposure to treatments. Lignotubers (i.e., resprouting organs) of harvested E. tereticornis seedlings that were retained in situ for an additional year were used to examine resprouting response. The likelihood of resprouting and biomass of resprouts increased with lignotuber volume, which was not itself affected by eCO2. The presence of herbaceous competitors and defoliation by invertebrates and pathogens were found to greatly reduce growth and/or resprouting response of seedlings. Our findings do not support the hypothesis that future increases in atmospheric [CO2] will, by itself, promote woody plant recruitment in eucalypt-dominated temperate grassy woodlands.

Palliative chemotherapy after failure of high-dose chemotherapy in breast cancer--toxicity and efficacy.

We evaluated the toxicity and efficacy of the first palliative chemotherapy regimen after failure of high-dose chemotherapy in 148 patients with primary or metastatic breast cancer treated with high-dose chemotherapy (one full dose CTC, (cyclophosphamide 6000 mg/m2, thiotepa 480 mg/m2, carboplatin 1600 mg/m2) or multiple courses CTC or 'tiny' CTC (tCTC) (two-thirds of the agents of the full-dose regimen), all divided over 4 days). After a median follow-up time of 46.8 (range 1-120) months, 79 patients had a relapse or progressive disease and 41 patients were treated with palliative chemotherapy. The most commonly used regimens were classical CMF (n = 13), docetaxel (n = 16) and less frequently anthracycline (n = 4), paclitaxel (n = 5), capecitabine (n = 2) and vinorelbine (n = 2). In both the CMF and docetaxel group, 3 patients required a dose reduction because of hematological toxicity. Objective responses were seen with CMF (23%) and docetaxel (69%) with a median duration of 161 (range 28-481) and 196 (range 62-437) days, respectively. We found no relationship of toxicity and response with treatment-free interval after high-dose chemotherapy. This report shows that conventional-dose palliative chemotherapy regimens may be safe and effective after failure of high-dose chemotherapy.

Autosomal recessive phosphorylase kinase deficiency in liver, caused by mutations in the gene encoding the beta subunit (PHKB).

The association of autosomal recessive phosphorylase kinase deficiency in liver of a 3 1/2-year-old female child with mutations in the gene encoding the common part of the beta subunit of phosphorylase kinase is reported. The proband had a severe deficiency of phosphorylase kinase in liver, while the phosphorylase kinase activity in erythrocytes was only slightly diminished. She had no symptoms of muscle involvement. The complete coding sequences of the liver gamma subunit and of the beta subunit of phosphorylase kinase of the proband were analyzed for the presence of mutations, by either reverse-transcribed PCR or SSCP analysis. Three deviations from the normal sequence were found in the region encoding the common part of the beta subunit of phosphorylase kinase-namely, a 1827G-->A (W609X) transition, a 2309A-->G (Y770C) transition, and a deletion of nucleotides 2896-2911-whereas no mutations were detected in the sequence encoding the liver gamma subunit of phosphorylase kinase. The 1827G-->A mutation and the deletion both result in the formation of early stop codons. Investigation of DNA showed that the deletion is caused by a splice-acceptor site mutation (IVS30(-1),g-->t). Family analysis revealed that the 1827G-->A and IVS30(-1),g-->t substitutions are located on different parental chromosomes and that compound heterozygosity for these mutations segregates with the disease. The 2309A-->G mutation was detected in 2%-3% of the normal population. Thus, it is concluded that the deficiency of phosphorylase kinase in this proband is caused by compound heterozygosity for the 1827G-->A and the IVS30(-1),g-->t mutations and that the 2309A-->G mutation is a polymorphism. This implies that a defect in the sequence encoding the common part of the beta subunit of phosphorylase kinase may present as liver phosphorylase kinase deficiency.