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A previous study revealed a positive correlation between heat-induced damage to photosynthetic membranes (thylakoid membranes) and chlorophyll loss. In this study, we exploited this correlation and developed a model for predicting thermal damage to thylakoids. Prediction is based on estimation of the ratio of constant chlorophyll a fluorescence (O) and the peak of variable fluorescence (P) (O/P). The model was developed using 12 cultivars of hexaploid winter wheat (Triticum aestivum L.). It was tested in six genotypes of hexaploid wheat, 25 genotypes of tetraploid wheat (T. turgidum L.), and 20 genotypes of maize (Zea mays L.). Predictive ability was assessed by analyzing the relationship between the predicted and measured O/P. The model adequately predicted O/P and thereby the heat stability of thylakoid membranes in all genotype groups with high coefficients of determination ([r.sup.2] > 0.80). This model could be used as an easy and inexpensive means for detection of the structural and functional state of photosynthetic membranes in wheat and maize, and possibly other crops, in hot environments.

Determining mechanisms associated with heat tolerance and identifying screening methods are vital for improvement of heat tolerance in plants. The objectives of this study were to investigate the relationship between the heat stability of thylakoids and loss of chlorophyll in winter wheat (Triticum aestivum L.) under heat stress, and to examine whether chlorophyll loss can be used as an indicator of heat tolerance in wheat. We assessed heat tolerance and measured chlorophyll content in 12 cultivars of winter wheat at flowering stage during exposure to 16-d-long heat stress. Heat tolerance was assessed using fluorescence to determine the heat stability of thylakoids, and chlorophyll content was measured with a chlorophyll meter. Experiments were conducted under controlled conditions. Heat stress caused damage to thylakoids in all cultivars as indicated by the increase in the ratio of constant fluorescence (O) and the peak of variable fluorescence (P). Heat stress also caused a decline in chlorophyll content in most cultivars. A strong negative correlation between heat-induced increases in O/P and chlorophyll content was seen. The results suggest that heat-induced damage to thylakoids and chlorophyll loss are closely associated in winter wheat. Measurements of chlorophyll content with a chlorophyll meter could be useful for high throughput screening for heat tolerance in wheat.

Reperfusion of ischemic tissue induces significant tissue damage in multiple conditions, including myocardial infarctions, stroke, and transplantation. Although not as common, the mortality rate of mesenteric ischemia/reperfusion (IR) remains >70%. Although complement and naturally occurring Abs are known to mediate significant damage during IR, the target Ags are intracellular molecules. We investigated the role of the serum protein, β2-glycoprotein I as an initiating Ag for Ab recognition and β2-glycoprotein I (β2-GPI) peptides as a therapeutic for mesenteric IR. The time course of β2-GPI binding to the tissue indicated binding and complement activation within 15 min postreperfusion. Treatment of wild-type mice with peptides corresponding to the lipid binding domain V of β2-GPI blocked intestinal injury and inflammation, including cellular influx and cytokine and eicosanoid production. The optimal therapeutic peptide (peptide 296) contained the lysine-rich region of domain V. In addition, damage and most inflammation were also blocked by peptide 305, which overlaps with peptide 296 but does not contain the lysine-rich, phospholipid-binding region. Importantly, peptide 296 retained efficacy after replacement of cysteine residues with serine. In addition, infusion of wild-type serum containing reduced levels of anti-β2-GPI Abs into Rag-1(-/-) mice prevented IR-induced intestinal damage and inflammation. Taken together, these data suggest that the serum protein β2-GPI initiates the IR-induced intestinal damage and inflammatory response and as such is a critical therapeutic target for IR-induced damage and inflammation.

To determine the mycorrhizal status and to identify the fungi colonising the roots of the plants, common buckwheat (Fagopyrum esculentum) and tartary buckwheat (F. tataricum) were inoculated with an indigenous fungal mixture from a buckwheat field. Root colonisation was characterised by the hyphae and distinct microsclerotia of dark septate endophytes, with occasional arbuscules and vesicles of arbuscular mycorrhizal fungi. Sequences of arbuscular mycorrhizal fungi colonising tartary buckwheat clustered close to the Glomus species group A. Sequences with similarity to the Ceratobasidium/Rhizoctonia complex, a putative dark septate endophyte fungus, were amplified from the roots of both common and tartary buckwheat. To the best of our knowledge, this is the first report of arbuscular mycorrhizal colonisation in tartary buckwheat and the first molecular characterisation of these fungi that can colonise both of these economically important plant species.