Effects of physioball and conventional floor exercises on early phase adaptations in back and abdominal core stability and balance in women

The purpose of this study was to compare the effects of 5 weeks of physioball core stability and balance exercises with conventional floor exercises in women. The experimental group (n = 15) performed curl-ups and back extensions on the physioball while the control group (n = 15) performed the same exercises on the floor. Baseline and post-training tests included electromyography (EMG) recordings of the rectus abdominus and erector spinae muscles; abdominal, back, and knee strength measurements with the Cybex Norm System; and 2 unilateral stance balance tests. The physioball group was found to have significantly greater mean change in EMG flexion and extension activity (p = 0.04 and p = 0.01, respectively) and greater balance scores (p < 0.01) than the floor exercise group. No significant changes (p > 0.05) were observed for heart rate or Cybex strength measurements. Early adaptations in a short-term core exercise program using the physioball resulted in greater gains in torso balance and EMG neuronal activity in previously untrained women when compared to performing exercises on the floor.     

Association of polymorphisms in the human IL4 and IL5 genes with atopic bronchial asthma and severity of the disease

Two polymorphisms in the IL4 (G/C 3'-UTR) and IL5 (C-703T) genes were studied in a sample of families whose probands had atopic bronchial asthma (BA) (66 families, n = 183) and in a group of non-cognate individuals with the severe form of the disease (n = 34). The samples were collected from the Russian population in the city of Tomsk (Russia). Using the transmission/disequilibrium test (TDT), a significant association of allele C-703 IL5 with BA was established (TDT = 4.923, p = 0.007 +/- 0.0007). The analysis of 40 individuals with mild asthma and 49 patients with the severe form of the disease revealed a negative association of genotype GG IL4 (OR = 0.39, 95% CI = 0.15-0.99, p = 0.035), and also a trend towards a positive association of the GC IL4 genotype (OR = 2.52, 95% CI = 0.98-6.57, p = 0.052) with mild BA. There was a concordance of the clinical classification of BA severity with the 'genotype' (McNemar's chi(2) test with continuity correction constituted 0.03, d.f. = 1, p = 0.859). These results suggest that polymorphisms in the IL4 and IL5 genes contribute to the susceptibility to atopic BA and could determine the clinical course of the disease.     

Restoration of defective cross talk in ssi2 mutants: role of salicylic acid, jasmonic acid, and fatty acids in SSI2-mediated signaling

The Arabidopsis mutants ssi2 and fab2 are defective in stearoyl ACP desaturase, which causes altered salicylic acid (SA)- and jasmonic acid (JA)-mediated defense signaling. Both ssi2 and fab2 plants show spontaneous cell death, express PR genes constitutively, accumulate high levels of SA, and exhibit enhanced resistance to bacterial and oomycete pathogens. In contrast to constitutive activation of the SA pathway, ssi2 and fab2 plants are repressed in JA-mediated induction of the PDF1.2 gene, which suggests that the SSI2-mediated signaling pathway modulates cross talk between the SA and JA pathways. In this study, we have characterized two recessive nonallelic mutants in the ssi2 background, designated as rdc (restorer of defective cross talk) 2 and rdc8. Both ssi2 rdc mutants are suppressed in constitutive SA signaling, show basal level expression of PR-1 gene, and induce high levels of PDF1.2 in response to exogenous application of JA. Interestingly, while the rdc8 mutation completely abolishes spontaneous cell death in ssi2 rdc8 plants, the ssi2 rdc2 plants continue to show some albeit reduced cell death. Fatty acid (FA) analysis showed a reduction in 16:3 levels in ssi2 rdc8 plants, which suggests that this mutation may limit the flux of FAs into the prokaryotic pathway of glycerolipid biosynthesis. Both rdc2 and rdc8 continue to accumulate high levels of 18:0, which suggests that 18:0 levels were responsible for neither constitutive SA signaling nor repression of JA-induced expression of the PDF1.2 gene in ssi2 plants. We also analyzed SA and JA responses of the fab2-derived shs1 mutant, which accumulates levels of 18:0 over 50% lower than those in the fab2 plants. Even though fab2 shs1 plants were morphologically bigger than fab2 plants, they expressed PR genes constitutively, showed HR-like cell death, and accumulated elevated levels of SA. However, unlike the ssi2 rdc plants, fab2 shs1 plants were unable to induce high levels of PDF1.2 expression in response to exogenous application of JA. Together, these results show that defective cross talk in ssi2 can be restored by second site mutations and is independent of morphological size of the plants, cell death, and elevated levels of 18:0.     

The NADP-Dependent Methylene Tetrahydromethanopterin Dehydrogenase in Methylobacterium extorquens AM1

An NADP-dependent methylene tetrahydromethanopterin (H₄MPT) dehydrogenase has recently been proposed to be involved in formaldehyde oxidation to CO₂ in Methylobacterium extorquens AM1. We report here on the purification of this novel enzyme to apparent homogeneity. Via the N-terminal amino acid sequence, it was identified to be the mtdA gene product. The purified enzyme catalyzed the dehydrogenation of methylene H₄MPT with NADP⁺ rather than with NAD⁺, with a specific activity of approximately 400 U/mg of protein. It also catalyzed the dehydrogenation of methylene tetrahydrofolate (methylene H₄F) with NADP⁺. With methylene H₄F as the substrate, however, the specific activity (26 U/mg) and the catalytic efficiency (V_max/K_m) were approximately 20-fold lower than with methylene H₄MPT. Whereas the dehydrogenation of methylene H₄MPT (E₀ = −390 mV) with NADP⁺ (E₀ = −320 mV) proceeded essentially irreversibly, the dehydrogenation of methylene H₄F (E₀ = −300 mV) was fully reversible. Comparison of the primary structure of the NADP-dependent dehydrogenase from M. extorquens AM1 with those of methylene H₄F dehydrogenases from other bacteria and eucarya and with those of methylene H₄MPT dehydrogenases from methanogenic archaea revealed only marginally significant similarity (<15%).     

Distribution, biomass and primary production of an Ahnfeltia tobuchiensis (Ahnfeltiales, Rhodophyta) population in the Bay of Izmena, Kunashir Island

Regularities of distribution and primary production of an Ahnfeltia tobuchiensis (Kanno et Matsubara) Mak. population, an agar-containing red alga, were studied in the Bay ot Izmena. Experiments were conducted in a flow-through system under conditions similar to algal habitats. The population of A. tobuchiensis unattached to the ground may be from a few centimeters to as much as 1 m thick. It has been shown that only the upper part of a stratum 15–20 cm thick receives a sufficient amount ot light to realize its production potential. While 15–20% of photosynthetically active radiation (PAR) of that falling on the water surface reaches the stratum surface, only 0.1% of PAR from that falling on the water surface penetrates through stratum 15 cm thick. It has been shown for A. tobuchiensis that its photosynthetic rate curve during the daytime mainly follows the PAR intensity curve. The highest values of photosynthetic rate have been measured in the afternoon when PAR reaches its maximum. It is noted that a stratum 15–20 cm thick has peak values ot net primary production (NPP) which averages 3.2 g C m^?2 day^?1. The total area of A. tobuchiensis population was 23.4 km², and its biomass was 125 000 tons in this area. On average, the NPP of the A. tobuchiensis population made up in summer and in autumn was 46.8 and 25.0% of its biomass, respectively.     

N-Terminal 2,3-diaminopropionic acid (Dap) peptides as efficient methylglyoxal scavengers to inhibit advanced glycation endproduct (AGE) formation

2,3-Diaminopropionic acid (Dap) and N-terminal Dap peptides have been found to inhibit in vitro protein-modifications by methylglyoxal (MG), one of the highly reactive α-dicarbonyl compounds. MG scavenging potency of the newly synthesized N-terminal Dap peptides is demonstrated by RP-HPLC, SDS–PAGE and non-denaturing PAGE analysis, assays for enzymatic activity and cell viability study and was compared with that of known AGE inhibitors, such as aminoguanidine, pyridoxamine, metformin and carnosine. Two addition products of MG and l-Dap-l-Leu are separated by HPLC and their chemical structures are characterized by ¹H and ¹³C NMR spectroscopy to indicate that both of them are pyrazines derived from 2 molecules of MG and 1 molecule of l-Dap-l-Leu. Mutagenic activities of l-Dap-l-Leu and l-Dap-l-Val and their metabolites according to the Ames assay are found to be negative.     

Eukaryote-specific motif of ribosomal protein S15 neighbors A site codon during elongation and termination of translation

The eukaryotic ribosomal protein S15 is a key component of the decoding site in contrast to its prokaryotic counterpart, S19p, which is located away from the mRNA binding track on the ribosome. Here, we determined the oligopeptide of S15 neighboring the A site mRNA codon on the human 80S ribosome with the use of mRNA analogues bearing perfluorophenyl azide-modified nucleotides in the sense or stop codon targeted to the 80S ribosomal A site. The protein was cross-linked to mRNA analogues in specific ribosomal complexes that were obtained in the presence of eRF1 in the experiments with mRNAs bearing stop codon. Digestion of modified S15 with various specific proteolytic agents followed by identification of the resulting modified oligopeptides showed that cross-link was in C-terminal fragment in positions 131–145, most probably, in decapeptide 131-PGIGATHSSR-140. The position of cross-linking site on the S15 protein did not depend on the nature of the A site-bound codon (sense or stop codon) and on the presence of polypeptide chain release factor eRF1 in the ribosomal complexes with mRNA analogues bearing a stop codon. The results indicate an involvement of the mentioned decapeptide in the formation of the ribosomal decoding site during elongation and termination of translation. Alignment of amino acid sequences of eukaryotic S15 and its prokaryotic counterpart, S19p from eubacteria and archaea, revealed that decapeptide PGIGATHSSR in positions 131–140 is strongly conserved in eukaryotes and has minor variations in archaea but has no homology with any sequence in C-terminal part of eubacterial S19p, which suggests involvement of the decapeptide in the translation process in a eukaryote-specific manner.     

A Possible Role for Exocytosis in Aflatoxin Export in Aspergillus parasiticus

Filamentous fungi synthesize bioactive secondary metabolites with major human health and economic impacts. Little is known about the mechanisms that mediate the export of these metabolites to the cell exterior. Aspergillus parasiticus synthesizes aflatoxin, a secondary metabolite that is one of the most potent naturally occurring carcinogens known. We previously demonstrated that aflatoxin is synthesized and compartmentalized in specialized vesicles called aflatoxisomes and that these subcellular organelles also play a role in the export process. In the current study, we tested the hypothesis that aflatoxisomes fuse with the cytoplasmic membrane to facilitate the release of aflatoxin into the growth environment. Microscopic analysis of A. parasiticus grown under aflatoxin-inducing and non-aflatoxin-inducing conditions generated several lines of experimental evidence that supported the hypothesis. On the basis of the evidence, we propose that export of the mycotoxin aflatoxin in Aspergillus parasiticus occurs by exocytosis, and we present a model to illustrate this export mechanism.Secondary metabolites are chemically diverse natural products synthesized by plants, fungi, bacteria, algae, and animals. Secondary metabolites have an enormous impact on humans. Antibiotics, for example, are essential elements of the multibillion-dollar pharmaceutical industry, whereas mycotoxins cause hundreds of millions of dollars in damage to agriculture annually (11, 15). These chemicals help the producing organism to survive nutrient limitation (16). They also contribute to cellular defense mechanisms and development (11, 12), reduce cellular oxidative stress (10), and help maintain cellular homeostasis by regulating carbon flow in the cell (17).Many fungal secondary metabolites are exported outside the cell; examples include antibiotics and mycotoxins (3, 14). We and others conducted extensive studies on the regulation of fungal secondary metabolism at the molecular (11, 15) and cellular (3, 7) levels. However, little is known about the mechanisms that mediate secondary metabolite export or why export occurs.The filamentous fungus Aspergillus parasiticus produces aflatoxin, a secondary metabolite and the most potent naturally occurring carcinogen known. More than 90% of aflatoxin is exported to the cell exterior (3), making A. parasiticus an excellent model for studying secondary metabolite export. We recently demonstrated that specialized trafficking vesicles called aflatoxisomes play a key role in aflatoxin synthesis and export (3). As synthesis initiates, vesicle-vacuole fusion is downregulated by the global regulator Velvet, resulting in the accumulation of aflatoxisomes which contain at least the last two functional enzymes in the aflatoxin pathway and sequester aflatoxin (3). Treatments that block vesicle-vacuole fusion increase the number of aflatoxisomes, increase the quantity of aflatoxin accumulated in aflatoxisomes, and increase aflatoxin export to the cell exterior (3). On the basis of these previous observations, we hypothesized that aflatoxisomes play a direct role in aflatoxin export.Vesicle-mediated export could theoretically occur by one (or more) of at least three mechanisms (Fig. 1). (i) Vesicles pass across the cytoplasmic membrane intact and “shuttle” their contents into the external environment. This proposed mechanism mediates virulence factor release in Cryptococcus neoformans and Histoplasma capsulatum (1) during pathogenesis. (ii) Vesicles fuse to the cytoplasmic membrane and “pump” vesicle contents to the exterior using transporter proteins similar to those that mediate resistance to antifungal agents (4, 5). (iii) Vesicles fuse with the cytoplasmic membrane, which evaginates, bursts, and “blasts” vesicle contents to the exterior. This process is similar to exocytosis, a proposed secretory mechanism for specific proteins in filamentous fungi (18). We conducted the current study to determine which, if any, of these possible mechanisms most accurately reflects the process of aflatoxin export in A. parasiticus.Open in a separate windowFig. 1.Theoretical models for vesicle-mediated export. Aflatoxigenic vesicles (aflatoxisomes) arise due to downregulation of tethering complex (Tc) activity mediated by VeA (1). Aflatoxin synthesized in aflatoxisomes could theoretically be released to the cell exterior by one or more of three mechanisms: the shuttle (in which aflatoxisomes shuttle cargo across cytoplasmic membrane), pump (in which transmembrane transporter [Tp] proteins mediate the release of secondary metabolites as vesicles adhere to the inner surface of the cytoplasmic membrane), and burst-and-blast (in which vesicles protrude from the cell surface and blast their cargo into the medium) mechanisms. PM, plasma membrane.