Competition for L-lactate betweenDesulfovibrio,Veillonella, andAcetobacterium species isolated from anaerobic intertidal sediments

Almost equal numbers ofDesulfovibrio, Veillonella, andAcetobacterium species were found in agar shake dilutions of anaerobic intertidal brackish sediments applying L-lactate as the only energy source and sulfate as electron acceptor. Pure cultures of these bacteria were studied in more detail in batch cultures as well as in L-lactate-limited chemostats. The maximal specific growth rates on L-lactate were determined in washout experiments and amounted to 0.16, 0.30, and 0.06 h^–1 forDesulfovibrio baculatus H.L21,Veillonella alcalescens NS.L49, andAcetobacterium NS.L40, respectively. Competition for L-lactate was studied in energy-limited chemostats at a dilution rate of 0.02 h^–1.D. baculatus H.L21 turned out to be the best competitor at low L-lactate concentrations provided that sufficient sulfate and iron were present.V. alcalescens NS.L49 was favored by the absence of sulfate and iron. Coexistence ofD. baculatus H.L21 andV. alcalescens NS.L49 was observed in a L-lactate-limited chemostat with additional sulfate and citrate. Syntrophic growth ofV. alcalescens NS.L49 andAcetobacterium NS.L40 occurred in a L-lactate-limited chemostat in the absence of sulfate. No coexistence betweenD. baculatus H.L21 andAcetobacterium NS.L40 was observed in a L-lactate-limited chemostat without sulfate. Addition of calcium-saturated illite to an energy-limited mixed culture ofV. alcalescens NS.L49 andAcetobacterium NS.L40 induced iron limitation and subsequent washout of theAcetobacterium species. Finally, the ecological niches of the 3 species in relation to the consumption of lactate were discussed.     

Expression of the potato leafroll luteovirus coat protein gene in transgenic potato plants inhibits viral infection

Transgenic potato plants, cultivar Désirée, were produced that contained the coat protein gene of potato leafroll luteovirus (PLRV). The transformed potato plants expressed the PLRV coat protein (CP) RNA sequences but accumulation of coat protein in transgenic tissues could not be detected. Upon inoculation with PLRV, the PLRV CP RNA expressing potato plants showed a reduced rate of virus multiplication.     

T 4 -mediated v-gene reactivation of UV-irradiated phage Ti, and its comparison with host-cell reactivation

Soaked seeds of Vicia faba were irradiated with 800 or 400 R, or two 400-R exposures, both with VAC (vacuum) but one with a concomitant treatment of CHM (cycloheximide) (I μg/ml). The chromosome aberration yields from each regimen varied with fixation time such that a unique and characteristic aberration yield for each regimen relative to the others was not obtained. Were single fixations employed one could obtain yields which would indicate no, some, or maximum repair. A single fixation would lead to an incorrect estimation of chromosome damage repair.     

Beat shock proteins and atrial fibrillation

In this mini-review, the role of heat shock proteins in susceptability to induction of atrial fibrillation (AF) or in the process of AF is discussed. AF is the most common arrhythmia in humans, is self-perpetuating in nature and hence tends to become more persistent in time. Some studies show a correlation between high Hsp70 (HspA1A) expression in cardiac tissue and a reduced susceptability to induction of postoperative AF. Expression of Hsp70, Hsc70 (HspA8), Hsp40 (DnaJB1), Hsp60 (HspD1), Hsp90 (HspC1) was not associated with progression of AF. However, both correlative studies in human and experimental studies suggest that Hsp27 (HspB1) may delay progression of AF to the more permanent forms and hence Hsp27 might be referred to as a "Beat shock protein".     

Overexpression of Cystathionine γ-Lyase Suppresses Detrimental Effects of Spinocerebellar Ataxia Type 3

Spinocerebellar ataxia type 3 (SCA3) is a polyglutamine (polyQ) disorder caused by a CAG repeat expansion in the ataxin-3 (ATXN3) gene resulting in toxic protein aggregation. Inflammation and oxidative stress are considered secondary factors contributing to the progression of this neurodegenerative disease. There is no cure that halts or reverses the progressive neurodegeneration of SCA3. Here we show that overexpression of cystathionine γ-lyase, a central enzyme in cysteine metabolism, is protective in a Drosophila model for SCA3. SCA3 flies show eye degeneration, increased oxidative stress, insoluble protein aggregates, reduced levels of protein persulfidation and increased activation of the innate immune response. Overexpression of Drosophila cystathionine γ-lyase restores protein persulfidation, decreases oxidative stress, dampens the immune response and improves SCA3-associated tissue degeneration. Levels of insoluble protein aggregates are not altered; therefore, the data implicate a modifying role of cystathionine γ-lyase in ameliorating the downstream consequence of protein aggregation leading to protection against SCA3-induced tissue degeneration. The cystathionine γ-lyase expression is decreased in affected brain tissue of SCA3 patients, suggesting that enhancers of cystathionine γ-lyase expression or activity are attractive candidates for future therapies.     

A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects

Many chronic pulmonary diseases are associated with pulmonary hypertension (PH) and pulmonary vascular remodeling, which is a term that continues to be used to describe a wide spectrum of vascular abnormalities. Pulmonary vascular structural changes frequently increase pulmonary vascular resistance, causing PH and right heart failure. Although rat models had been standard models of PH research, in more recent years the availability of genetically engineered mice has made this species attractive for many investigators. Here we review a large amount of data derived from experimental PH reports published since 1996. These studies using wild-type and genetically designed mice illustrate the challenges and opportunities provided by these models. Hemodynamic measurements are difficult to obtain in mice, and right heart failure has not been investigated in mice. Anatomical, cellular, and genetic differences distinguish mice and rats, and pharmacogenomics may explain the degree of PH and the particular mode of pulmonary vascular adaptation and also the response of the right ventricle.     

Modifier gene study of meconium ileus in cystic fibrosis: statistical considerations and gene mapping results

Cystic fibrosis (CF) is a monogenic disease due to mutations in the CFTR gene. Yet, variability in CF disease presentation is presumed to be affected by modifier genes, such as those recently demonstrated for the pulmonary aspect. Here, we conduct a modifier gene study for meconium ileus (MI), an intestinal obstruction that occurs in 16–20% of CF newborns, providing linkage and association results from large family and case–control samples. Linkage analysis of modifier traits is different than linkage analysis of primary traits on which a sample was ascertained. Here, we articulate a source of confounding unique to modifier gene studies and provide an example of how one might overcome the confounding in the context of linkage studies. Our linkage analysis provided evidence of a MI locus on chromosome 12p13.3, which was segregating in up to 80% of MI families with at least one affected offspring (HLOD = 2.9). Fine mapping of the 12p13.3 region in a large case–control sample of pancreatic insufficient Canadian CF patients with and without MI pointed to the involvement of ADIPOR2 in MI (p = 0.002). This marker was substantially out of Hardy–Weinberg equilibrium in the cases only, and provided evidence of a cohort effect. The association with rs9300298 in the ADIPOR2 gene at the 12p13.3 locus was replicated in an independent sample of CF families. A protective locus, using the phenotype of no-MI, mapped to 4q13.3 (HLOD = 3.19), with substantial heterogeneity. A candidate gene in the region, SLC4A4, provided preliminary evidence of association (p = 0.002), warranting further follow-up studies. Our linkage approach was used to direct our fine-mapping studies, which uncovered two potential modifier genes worthy of follow-up.     

Mangrove-sponge associations: a possible role for tannins

A positive correlation between sponge coverage and tannin concentrations in prop roots of Rhizophora mangle L. has previously been reported. However, the ecological role of tannins within the mangrove sponge association remains speculative. This study investigated whether tannins play a role in sponge recruitment and assessed tannin and polyphenol production in R. mangle roots in response to sponge colonization. We demonstrated in a field experiment using artificial substrates with different tannin concentrations that tannins are positively involved in larval recruitment of the sponge Tedania ignis and that roots significantly enhanced tannin and polyphenolic content in response to natural and experimental sponge fouling. Differential recruitment in response to tannins may have been the result of a behavioral response in sponge larvae. It is also possible that tannins affected the structure of the fouling microbial biofilm on the artificial substrate, or tannins affected the post-settlement dynamics of sponge recruits. Elevations in concentrations of tannins and polyphenolic compounds upon coverage with sponges, combined with differential recruitment of T. ignis in response to differences in tannin concentrations, may indicate a positive feedback in recruitment. This may in part explain the typical heterogeneity in sponge coverage and community composition among roots.     

FK506, transforming growth factor-beta1 and mesangial matrix synthesis: parallels and differences compared with cyclosporine A

Cyclosporine A (CsA)-induced glomerulosclerosis is a well-described side effect of CsA treatment. Current evidence indicates that FK506 causes similar morphologic changes. Recently, we demonstrated that CsA up-regulates the expression of transforming growth factor-beta1 (TGF-beta1), its receptors type I (TbetaR-I) and type II (TbetaR-II), as well as related matrix protein synthesis in mesangial cells (MCs). Here, we assessed the effect of FK506 on the expression of TGF-beta1, TbetaR-I, TbetaR-II, fibronectin (FN) and plasminogen activator inhibitor type-1 (PAI-1) in MCs. Resting MCs were incubated with/without FK506. Time- and concentration-dependent expression was measured at the mRNA and protein level. Compared to untreated controls, FK506 stimulated TGF-beta1 mRNA (maximum at 8 h, 100 ng/mL: 2.13+/-0.15-fold, P<0.005) and protein expression (maximum at 96 h, 100 ng/mL: 1.96+/-0.29-fold, P<0.005). In contrast, TbetaR-I and TbetaR-II protein expression remained unchanged. Concerning matrix protein synthesis, FK506 slightly increased FN production (96 h, 100 ng/mL: 1.38+/-0.28-fold, P<0.05), but not PAI-1 production. These results indicate that, comparable to CsA, FK506 induced glomerulosclerosis is also due to a direct effect on mesangial matrix production, which is at least in part mediated via up-regulation of TGF-beta1 expression. The fact that, unlike CsA, FK506 does not increase the expression of TbetaR-I, TbetaR-II, and PAI-1, deserves further investigation.