Mapping a gene conferring resistance to <Emphasis Type="Italic">Wheat yellow mosaic virus</Emphasis> in European winter wheat cultivar ‘Ibis’ (<Emphasis Type="Italic">Triticum aestivum</Emphasis> L.)

Wheat yellow mosaic, caused by Wheat yellow mosaic virus (WYMV), is one of the most devastating soil-borne diseases of winter wheat (Triticum aestivum L.) in Japan. Yellow-striped leaves and stunted spring growth, symptomatic of WYMV infection, result in severe yield loss. A new putative WYMV resistance gene in the European wheat cultivar ‘Ibis’ was mapped in the cluster of microsatellite markers including Xcfd16, Xwmc41, Xcfd168 and Xwmc181 on the long arm of chromosome 2D at the distances of 2.0 cM, 4.0 cM, 7.1 cM and 12.4 cM, respectively. WYMV-resistant cultivars contained a common haplotype of the four markers, whereas moderately susceptible and susceptible cultivars did not. These results should be useful in marker-assisted selection for WYMV resistance in wheat.     

Changes in the plasma levels of several bone markers in newborn calves during the first two days of life

The fluctuations in the plasma levels of several bone markers were investigated in newborn calves. Experiment 1 monitored the postnatal changes in the plasma levels of tartrate-resistant acid phosphatase isoform 5b (TRAP5b), total alkaline phosphatase (t-ALP) and bone-specific alkaline phosphatase (BAP) in four calves. These markers increased significantly from 9−20 hr after the first colostrum-suckling compared with the values immediately after birth. Experiment 2 evaluated changes in the plasma TRAP5b, t-ALP, BAP and type I collagen cross-linked N-telopeptide (NTx) levels within 2 days post-birth in five calves with successful passive immunization via colostrum (non-deficient group) and five others with poor colostrum intake (deficient group). The non-deficient group had significantly higher plasma levels of the four parameters around 12 hr of life compared with the deficient group. The results suggest that the increase in plasma bone markers in calves in the first day of life is related to the colostrum intake.     

Experimental studies on the oxygen tension in the myocardium and changes of cardiac function in hypoxia

Using adult mongrel dogs, experiments were performed to elucidate the relationship between the changes in the myocardial oxygen tension (PmO2) in anoxia and disturbances of cardiac function. Dogs, forced to inspire 100% N2, suffered from a respiratory arrest after 5 min, and developed acute anoxia. However, by 100% O2 inhalation 2 min after the onset of the respiratory arrest, the anoxia rapidly resolved. The arterial oxygen tension (PaO2), left intra ventricular oxygen tension (PLVO2) and PmO2 showed the most pronounced fall 2 min after the respiratory arrest induced by N2 inhalation. The arterial carbon deoxide tension (PaCO2) decreased until the respiratory arrest, after which it started to rise. When inhalation of 100% O2 was initiated at the anoxia, the PaO2, PLVO2 and PmO2 recovered within 1 min followed by a rise beyond the baseline value. Left ventricular end-diastolic pressure (LVEDP), left atrial mean pressure (LAm), left ventricular systolic pressure (LVSP), aortic mean pressure (Aom), maximum rate of force development by left ventricle (LVmax.dp/dt), total peripheral resistance (TPR), cardiac output (CO) and heart rate (HR) were measured. At the onset of anoxia, these parameters decreased sharply. When inhalation of 100% O2 was initiated within 2 min of the respiratory arrest, these disturbances of cardiac function recovered rapidly. The fall of PmO2 plays an important role in the impairment of cardiac function.     

Experimental studies of the load reducing effects of nitroglycerin in heart failure

The load-reducing effect of nitroglycerin (NTG), a vasodilator, was studied in dogs with heart failure. The chordae tendineae of the mitral valve were transected to induce acute mitral regurgitation (MR) for hemodynamic evaluation. By such surgical treatment, preload indices such as left ventricular end-diastolic pressure (LVEDP) and left atrial pressure (LAP) increased significantly, and subsequent cardiac dysfunction and heart failure were indicated by another decrease in stroke volume, myocardial contractility, forward flow, and myocardial oxygen consumption. To dogs with artificially established acute MR, 3 micrograms/kg/min of NTG was administered intra-arterially by means of a continuous infusion, that resulted in decrease of LVEDP, LAP and central venous pressure (CVP). Thus, a reduction of preload was determined. Simultaneously, afterload indices such as aortic systolic pressure (Aos), aortic mean pressure (Aom) and total peripheral resistance (TPR) decreased remarkably. Afterload reduction depended on the amount of venous return; therefore, an extra-corporeal circulation system was applied in order to supply a constant venous return before NTG administration. This caused a significant decrease in aortic diastolic pressure (Aod), Aos, Aom, left ventricular systolic pressure (LVSP) and TPR, and an increase in myocardial contractility and cardiac output. This suggested that afterload reduction might be realized by the vasodilatory effect of NTG on the resistance vessels.     

Studies on BHC isomers and related compounds: Penetration and translocation of BHC isomers in the cockroach and their correlation with physicochemical properties

Penetration of BHC isomers through the integument of Periplaneta americana (L.) is a composite of several first-order events. Translocation and accumulation in the head appears to be a zero-order function. The correlation of some of the biological properties with physicochemical properties such as partition coefficients and binding constants are discussed.     

Comparative insecticidal activities and metabolic rates of lindane and its hexadeuterio-analog

Hexadeuterio-lindane(γ-BHC-d₆) was several times as toxic as lindane against the mosquito (Culex pipiens pallens), house fly (Musca domestica), German cockroach (Blattella germanica) and American cockroach (Periplaneta americana). The neuroexcitatory activity of these two compounds did not differ. Lindane was considerably synergized by piperonyl butoxide, but lindane-d₆ was not. A large isotope effect was observed in the in vivo breakdown of lindane-d₆. Thus, the intrinsic toxicities of both compounds are equivalent. The difference in insecticidal activity seems to be due to the different rates of detoxifying biodegradation caused by the kinetic deuterium isotope effect.     

Oxidative metabolism of lindane and its isomers with microsomes from rat liver and house fly abdomen

Lindane and other hexachlorocyclohexane isomers produced 2,4,6-trichlorophenol as the major oxidative metabolite when incubated in the presence of NADPH under aerobic condition. A mechanism for the formation of 2,4,6-trichlorophenol is proposed, which includes direct oxygenation of the cyclohexane ring. The proposed mechanism is supported by data from studies of model chemical reactions of the pentachlorocyclohexanol isomers. Pathways leading to 1,2,4-trichlorobenzene, tetrachlorobenzene isomers, 2,4,5-trichlorophenol, and tetrachlorophenol isomers are discussed, and are considered to include the route through pentachlorocyclohexene and hexachlorocyclohexene. Reductive dechlorination of lindane under anaerobic condition was observed using microsomes and NADPH.     

Decreases in serum apolipoprotein C-III concentration in cows with ethionine-induced fatty liver

To monitor the serum concentration of apolipoprotein C-III (apoC-III), one of the functional apoproteins in lipid metabolism, in cows with ethionine-induced fatty liver, and to investigate the association of apoC-III with liver triglyceride (TG) content and serum biochemical variables, seven nonpregnant nonlactating Holstein cows (3 to 6 years old) were used. Five cows were treated with ethionine, an analogue of methionine, (days 0, 7 and 14). The remaining two controls received saline as the vehicle. Liver TG contents in the treated cows were increased markedly whenever administered, and significant increases were observed at days 14 (666.4%, 85.3 mg/g) and 21 (675.0%, 86.4 mg/g) compared with day 0. In controls, no significant changes in liver TG content and serum biochemical variables were observed during this experiment. The serum apoC-III concentration in the treated cows was decreased drastically after the first administration and fell to the lowest value at day 10 (76.2 microg/ml, 32% of day 0). The apoC-III was significantly (p<0.05) correlated with non-esterified fatty acids (r= -0.526), gamma-glutamyl transpeptidase (r= -0.407), total bilirubin (r= -0.464), positively with apolipoprotein B-100 (apoB-100, r=0.601) and cholesterol ester (r=0.449). Although apoB-100 concentrations were also reduced by the administrations, the concentrations tended to recover smoothly toward the next administration. The distinct difference in change between apoC-III and apoB-100 suggests that apoC-III may be regulated by other pathways, in addition to inhibiting the synthesis of apoproteins by ethionine.     

Inhibition by sulfatide of 21-kDa protein phosphorylation by protein kinase C in cow mammary gland and its reversal by phosphatidylserine

The effect of sulfatide, a sulfated sphingolipid, on phosphorylation of endogenous proteins by protein kinase C (PKC) was examined in cow mammary gland. Several proteins, including 21-kDa, 43-kDa and 56-kDa proteins in the cytosolic fraction, were found to be substrates for PKC by phosphorylation in the absence or presence of the cofactors 1-oleoyl-2-acetyl-sn-glycerol (OAG), phosphatidylserine (PS) and Ca2+. Sulfatide inhibited the 21-kDa phosphorylation, whereas it enhanced the 56-kDa and 43-kDa phosphorylation. Experiments were then conducted to examine whether other sphingolipids, including sphingosine, dihydrosphingosine, ceramides, galactocerebrosides, psychosine and sphingomyelin, modulated phosphorylation of the PKC substrates. Sphingosine, dihydrosphingosine and psychosine did not inhibit the 21-kDa phosphorylation; however, they enhanced the 56-kDa and 43-kDa phosphorylation. Ceramides, galactocerebrosides and sphingomyelin did not inhibit the 21-kDa or enhance the 56-kDa and 43-kDa phosphorylation. The inhibition by sulfatide of the 21-kDa phosphorylation was reversed by excess addition of PS, but not by OAG or Ca2+; whereas the enhancement by sulfatide, as well as sphingosine, dihydrosphingosine and psychosine, of 56-kDa and 43-kDa phosphorylation was not affected by PS, OAG or Ca2+. It is suggested that sulfatide is involved in the regulation of PKC-dependent phosphorylation by modulating the association of PKC substrates, in particular the 21-kDa protein, with membrane phospholipids in cow mammary gland.