Do secondary sexual dimorphism and female intolerance to drought influence the sex ratio and extinction risk of <Emphasis Type="Italic">Taxus baccata</Emphasis>?

Sex ratio and sexual dimorphism were studied in the dioecious tree Taxus baccata. We examined five populations of T. baccata in Poland and Ukraine to identify the differences between male and female individuals. The sex of all individuals, height and diameter, needle length and area, specific leaf area (SLA), the number of stomata rows, stomatal density, and content of carbon and nitrogen were measured to identify the differences between male and female individuals. The relationship between sex ratio and climatic conditions, age and population size were analysed using data collected from the field and the literature. Female trees were shorter than males, but needles of females were longer and had larger area. Although there were no differences among sexes in SLA, nitrogen and carbon concentration, we found a positive correlation between nitrogen concentration and SLA among females. The sex ratio changed with tree height within populations, and taller height classes were biased in favour of males. Regardless of population age, the percentage of females within populations was positively correlated with precipitation. Probably high reproductive effort caused female trees to lose in competition with males, and this loss may also be enhanced by lower drought tolerance in females and could contribute to risk of extinction for T. baccata. The continental geographic range of T. baccata may be restricted by limited occurrence of females, which demand higher water resources than males.     

A benzimidazole-based ruthenium(IV) complex inhibits Pseudomonas aeruginosa biofilm formation by interacting with siderophores and the cell envelope,and inducing oxidative stress

Pseudomonas aeruginosa biofilm-associated infections are a serious medical problem, and new compounds and therapies acting through novel mechanisms are much needed. Herein, the authors report a ruthenium(IV) complex that reduces P. aeruginosa PAO1 biofilm formation by 84%, and alters biofilm morphology and the living-to-dead cell ratio at 1?mM concentration. Including the compound in the culture medium altered the pigments secreted by PAO1, and fluorescence spectra revealed a decrease in pyoverdine. Scanning electron microscopy showed that the ruthenium complex did not penetrate the bacterial cell wall, but accumulated on external cell structures. Fluorescence quenching experiments indicated strong binding of the ruthenium complex to both plasmid DNA and bovine serum albumin. Formamidopyrimidine DNA N-glycosylase (Fpg) protein digestion of plasmid DNA isolated after ruthenium(IV) complex treatment revealed the generation of oxidative stress, which was further proved by the observed upregulation of catalase and superoxide dismutase gene expression.     

Oxidation of excited-state NADH and NAD dimer in aqueous medium involvement of O2− as a mediator in the presence of oxygen

It has been shown that direct excitation of NADH (or NADPH) in aqueous medium at 254 nm, or at wavelengths longer than 320 nm (where only the reduced nicotinamide moiety absorbs), leads to generation of NAD⁺ (or NADP⁺). The reaction proceeds both in the presence and absence of oxygen. Under aerobic conditions the reaction is accompanied by formation of H₂O₂ at a level equimolar with that of the NADH present in solution. On irradiation at wavelengths longer than 320 nm, conversion of NADH to enzymatically active NAD⁺ is about 75%. Under analogous irradiation conditions, the dimers (NAD)₂ and (NADP)₂ undergo disproportionation to NAD⁺ and NADP⁺, respectively, to the extent of 90%. Both physicochemical and enzymatic criteria were employed to formulate mechanisms for the photooxidation of NADH and the photodisproportionation of the dimer (NAD)₂.     

Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: A Randomized Controlled Trial

Background

An increased rate of brain atrophy is often observed in older subjects, in particular those who suffer from cognitive decline. Homocysteine is a risk factor for brain atrophy, cognitive impairment and dementia. Plasma concentrations of homocysteine can be lowered by dietary administration of B vitamins.

Objective

To determine whether supplementation with B vitamins that lower levels of plasma total homocysteine can slow the rate of brain atrophy in subjects with mild cognitive impairment in a randomised controlled trial (VITACOG, ISRCTN 94410159).

Methods and Findings

Single-center, randomized, double-blind controlled trial of high-dose folic acid, vitamins B₆ and B₁₂ in 271 individuals (of 646 screened) over 70 y old with mild cognitive impairment. A subset (187) volunteered to have cranial MRI scans at the start and finish of the study. Participants were randomly assigned to two groups of equal size, one treated with folic acid (0.8 mg/d), vitamin B₁₂ (0.5 mg/d) and vitamin B₆ (20 mg/d), the other with placebo; treatment was for 24 months. The main outcome measure was the change in the rate of atrophy of the whole brain assessed by serial volumetric MRI scans.

Results

A total of 168 participants (85 in active treatment group; 83 receiving placebo) completed the MRI section of the trial. The mean rate of brain atrophy per year was 0.76% [95% CI, 0.63–0.90] in the active treatment group and 1.08% [0.94–1.22] in the placebo group (P = 0.001). The treatment response was related to baseline homocysteine levels: the rate of atrophy in participants with homocysteine >13 µmol/L was 53% lower in the active treatment group (P = 0.001). A greater rate of atrophy was associated with a lower final cognitive test scores. There was no difference in serious adverse events according to treatment category.

Conclusions and Significance

The accelerated rate of brain atrophy in elderly with mild cognitive impairment can be slowed by treatment with homocysteine-lowering B vitamins. Sixteen percent of those over 70 y old have mild cognitive impairment and half of these develop Alzheimer''s disease. Since accelerated brain atrophy is a characteristic of subjects with mild cognitive impairment who convert to Alzheimer''s disease, trials are needed to see if the same treatment will delay the development of Alzheimer''s disease.

Trial Registration

Controlled-Trials.com ISRCTN94410159     

Effect of the Rho kinase inhibitor Y-27632 on the proteome of hearts with ischemia-reperfusion injury

Growing attention has been given to the role of the Rho kinase pathway in the development of heart disease and ischemia/reperfusion (I/R) injury. Y‐27632 is a Rho kinase inhibitor demonstrated to protect against I/R injury, but the exact mechanism by which it does so remains to be elucidated. The goal of this project was to determine new targets by which Y‐27632 can protect the heart against I/R injury. Isolated rat hearts were perfused under aerobic conditions or subjected to I/R in the presence or absence of Y‐27632. Administration of Y‐27632 (1 μM) before ischemia and during the first 10 min of reperfusion resulted in complete recovery of cardiac function. 2‐D electrophoresis followed by MS identified four proteins whose levels were affected by Y‐27632 treatment. Lactate dehydrogenase and glyceraldehyde‐3‐phosphate dehydrogenase were significantly increased in the Y‐27632 treated group, while creatine kinase was normalized to control levels. In addition, we found increased level of two different molecular fragments of ATP synthase, which were normalized by Y‐27632. This increase suggests that during ischemia ATP synthase is subjected to degradation. The changes in metabolic enzymes' levels and their regulation by Y‐27632 suggest that the cardioprotective effect of Y‐27632 involves increased energy production.