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121.
While the effect of habitat connectivity on local and regional diversity has been analysed in a number of studies, time-dependent dynamics in metacommunities have received comparatively little consideration. When local patches of a metacommunity are identical in environmental conditions but differ in initial community composition, dispersal among patches may result in homogenization of local communities. In a microcosm experiment with benthic ciliates, we tested the hypothesis that the effect of connectivity on diversity is time-dependent and only transitory, with the degree of connectivity affecting the time to homogenization but not the final outcome. Six microcosms were connected to a metacommunity with one of three levels of connectivity. The six patches differed in initial community composition but were identical in environmental conditions. We found a time-dependent and transitory effect of connectivity on local and regional richness and on local Shannon diversity, while Bray-Curtis dissimilarity and regional Shannon diversity were persistently affected by connectivity. Local richness increased and regional richness decreased with connectivity during the initial phase of the experiment but soon converged to similar values in all three connectivity treatments. Local Shannon diversity was unimodally related to time, with maximum diversity reached sooner with high than with medium or low connectivity. Eventually, however, local diversity converged to similar values irrespective of connectivity. At the regional scale, Shannon diversity was persistently lower with high than with low connectivity. While initial differences in community composition vanished with medium and high connectivity, they were maintained with low connectivity resulting in persistently high beta and regional diversity. The effect of connectivity on ciliate community composition translated down to the algal resource, as stronger dominance of the superior competitor with high and medium connectivity resulted in stronger depletion of the resource. 相似文献
122.
Background
Mitochondria are both the cellular powerhouse and the major source of reactive oxygen species. Coenzyme Q10 plays a key role in mitochondrial energy production and is recognized as a powerful antioxidant. For these reasons it can be argued that higher mitochondrial ubiquinone levels may enhance the energy state and protect from oxidative stress. Despite the large number of clinical studies on the effect of CoQ10 supplementation, there are very few experimental data about the mitochondrial ubiquinone content and the cellular bioenergetic state after supplementation. Controversial clinical and in vitro results are mainly due to the high hydrophobicity of this compound, which reduces its bioavailability.Principal Findings
We measured the cellular and mitochondrial ubiquinone content in two cell lines (T67 and H9c2) after supplementation with a hydrophilic CoQ10 formulation (Qter®) and native CoQ10. Our results show that the water soluble formulation is more efficient in increasing ubiquinone levels. We have evaluated the bioenergetics effect of ubiquinone treatment, demonstrating that intracellular CoQ10 content after Qter supplementation positively correlates with an improved mitochondrial functionality (increased oxygen consumption rate, transmembrane potential, ATP synthesis) and resistance to oxidative stress.Conclusions
The improved cellular energy metabolism related to increased CoQ10 content represents a strong rationale for the clinical use of coenzyme Q10 and highlights the biological effects of Qter®, that make it the eligible CoQ10 formulation for the ubiquinone supplementation. 相似文献123.
The expression of Ruminococcus flavefaciens 007S cellulases in different incubation time points (growth stages) and their substrate inducibility were analyzed by comparing the zymogram expression profiles of cultures grown on insoluble cellulose (Avicel) with cellobiose-grown cultures. The molecular weights of the enzymes were compared to (putative) cellulases encoded in the R. flavefaciens FD-1 genome. 相似文献
124.
Hornek R Pommerening-Röser A Koops HP Farnleitner AH Kreuzinger N Kirschner A Mach RL 《Journal of microbiological methods》2006,66(1):147-155
The gene encoding the active site of the ammonia monooxygenase (amoA) has been exploited as molecular marker for studying ammonia-oxidizing bacteria (AOB) diversity in the environment. Primers amplifying functional genes are often degenerated and therefore produce multiple band patterns, when analysed with the Denaturing gradient gel electrophoresis (DGGE) approach. To improve the DGGE band patterns we have designed new primer sets which contain inosine residues and are specific for the amoA gene. Primers were evaluated analysing pure AOB cultures and two habitats (wastewater treatment plant, soda pools). We found that the application of inosine primers helped to reduce the apparent complexity of the DGGE band pattern. Comparison of sequences from environmental samples using either degenerated or inosine containing amoA primers retrieved both identical and additional sequences. Both primer sets seem to be limited in their ability to detect the presence of all AOB by DGGE analyses. 相似文献
125.
Mitochondrial Complex I [NADH Coenzyme Q (CoQ) oxidoreductase] is the least understood of respiratory complexes. In this review
we emphasize some novel findings on this enzyme that are of relevance to the pathogenesis of neurodegenerative diseases. Besides
CoQ, also oxygen may be an electron acceptor from the enzyme, with generation of superoxide radical in the mitochondrial matrix.
The site of superoxide generation is debated: we present evidence based on the rational use of several inhibitors that the
one-electron donor to oxygen is an iron-sulphur cluster, presumably N2. On this assumption we present a novel mechanism of
electron transfer to the acceptor, CoQ. Complex I is deeply involved in pathological changes, including neurodegeneration.
Complex I changes are involved in common neurological diseases of the adult and old ages. Mitochondrial cytopathies due to
mutations of either nuclear or mitochondrial DNA may represent a useful model of neurodegeneration. In this review we discuss
Parkinson’s disease, where the pathogenic involvement of Complex I is better understood; the accumulated evidence on the mode
of action of Complex I inhibitors and their effect on oxygen radical generation is discussed in terms of the aetiology and
pathogenesis of the disease.
Special issue article in honor of Dr. Anna Maria Giuffrida-Stella. 相似文献
126.
Nenad Turk Zoran Milas Josip Margaletic Romana Turk Ljubo Barbic Dean Konjevic Sanja Peric Zrinka Stritof Vilim Staresina 《European Journal of Wildlife Research》2008,54(1):117-121
To determine whether some of the B. burgdorferi sensu lato genospecies associate with fat dormouse as a reservoir host, we investigated the prevalence of infection in questing
animals. A total of 45 adult fat dormice (30 female and 15 male) were captured by hunters during their hunting season in the
region of Gorski Kotar, Croatia. Dead animals were aseptically dissected, and the urinary bladder tissue was used for isolation
attempt and for deoxyribonucleic acid (DNA) extraction. Out of 45 DNA samples extracted from urine bladder tissue, we found
four (8.88%) to be polymerase chain reaction (PCR) positive. The RFLP analysis of the PCR product after cleavage with DraI and MseI distinguished between the three major genospecies: B. burgdorferi sensu stricto, B. garinii and B. afzelii. All positive samples were typed as B. afzelii with a unique DraI or MseI pattern. The results of the analysis of urinary bladder tissue samples culture for the presence of Borrelia were negative. Results showed that a prevalence of the Borrelia infection among population of fat dormice indicated their epizootiological involvement as a reservoir of Borrelia spirochetes. Furthermore, this work is an initial step in the investigation of the molecular epidemiology/epizootiology of
Lyme borreliosis in Croatia. 相似文献
127.
Anne Le Du Marc Lelorc'h Nelly Frydman Moncef Benkhalifa Serge Romana Michel Vekemans René Frydman Gérard Tachdjian 《Andrologie》2004,14(2):186-192
Men with a chromosomal translocation produce a significant percentage of unbalanced spermatozoa. In order to determine a correlation between chromosomal anomalies and apoptosis in human sperm, we analysed DNA fragmentation and meiotic segregation in sperm from men with a (13;14) Robertsonian translocation. We studied sperm from 12 (13;14) translocation carriers and 9 proven fertile men with a normal karyotype. Meiotic segregation of chromosomes 13 and 14 was analysed using dual-colour fluorescencein situ hybridization with locus-specific probes for chromosomes 13 and 14. Apoptosis in spermatozoa was measured byin situ TUNEL assay. The meiotic segregation study showed a significantly increased frequency of unbalanced spermatozoa for chromosomes 13 and 14 in (13;14) carriers (15.9%) compared to the control population (1.3%) (p=0.00016). The study of apoptosis showed an increase of DNA fragmentation in (13;14) carriers (34.9%) compared to the control population (13.8%) (p=0.0036). This increased apoptosis was observed in spermatozoa presenting an increase of unbalanced chromosomal anomalies concerning chromosomes 13 and 14, but with a predominance of balanced spermatozoa compared to the theoretical risk of meiotic segregation. These results suggest that apoptosis could be involved as a regulatory mechanism to eliminate unbalanced chromosomal spermatozoa in men with a (13;14) Robertsonian translocation. 相似文献
128.
The secretion of N-acetylglucosaminidase during germ-tube formation in Candida albicans 总被引:3,自引:0,他引:3
P A Sullivan N J McHugh L K Romana M G Shepherd 《Journal of general microbiology》1984,130(9):2213-2218
N-Acetylglucosaminidase was induced by either N-acetylglucosamine or N-acetylmannosamine in several strains of Candida albicans. Enzyme activity was not induced in a N-acetylglucosamine non-utilizing mutant which is unable to express the first three steps in the N-acetylglucosamine catabolic pathway. The enzyme, purified 500-fold, had a specific activity of 36.8 units (mg protein)-1 and catalysed the hydrolysis of p-nitrophenyl-beta-n-acetylglucosamine, N,N'-diacetylchitobiose and N,N',N"-triacetylchitotriose. No activity was observed toward colloidal chitin, hyaluronic acid or mucin. The cellular distribution of N-acetylglucosaminidase was determined by measuring in situ enzyme activity before and after acid treatment of intact cells. N-Acetylglucosaminidase (80-88% of the total cellular activity) was rapidly secreted to the periplasm when the enzyme was induced either during yeast growth at 28 degrees C or germ-tube formation at 37 degrees C. Export of the enzyme from the periplasm into the medium was fourfold greater during germ-tube formation, and after 6 h incubation the amount of enzyme released into the medium represented 70% of cell-associated enzyme activity. 相似文献
129.
Uroporphyrinogen decarboxylase: complete human gene sequence and molecular study of three families with hepatoerythropoietic porphyria. 总被引:4,自引:0,他引:4
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M. J. Moran-Jimenez C. Ged M. Romana R. Enriquez De Salamanca A. Taïeb G. Topi L. D'Alessandro H. de Verneuil 《American journal of human genetics》1996,58(4):712-721
A deficiency in uroporphyrinogen decarboxylase (UROD) enzyme activity, the fifth enzyme of the heme biosynthetic pathway, is found in patients with sporadic porphyria cutanea tarda (s-PCT), familial porphyria cutanea tarda (f-PCT), and hepatoerythropoietic porphyria (HEP). Subnormal UROD activity is due to mutations of the UROD gene in both f-PCT and HEP, but no mutations have been found in s-PCT. Genetic analysis has determined that f-PCT is transmitted as an autosomal dominant trait. In contrast, HEP, a severe form of cutaneous porphyria, is transmitted as an autosomal recessive trait. HEP is characterized by a profound deficiency of UROD activity, and the disease is usually manifest in childhood. In this study, a strategy was designed to identify alleles responsible for the HEP phenotype in three unrelated families. Mutations of UROD were identified by direct sequencing of four amplified fragments that contained the entire coding sequence of the UROD gene. Two new missense mutations were observed at the homoallelic state: P62L (proline-to-leucine substitution at codon 62) in a Portuguese family and Y311C (tyrosine-to-cysteine substitution at codon 311) in an Italian family. A third mutation, G281E, was observed in a Spanish family. This mutation has been previously described in three families from Spain and one from Tunisia. In the Spanish family described in this report, a paternal uncle of the proband developed clinically overt PCT as an adult and proved to be heterozygous for the G281E mutation. Mutant cDNAs corresponding to the P62L and Y311C changes detected in these families were created by site-directed mutagenesis. Recombinant proteins proved to have subnormal enzyme activity, and the Y311C mutant was thermolabile. 相似文献
130.
N Raich V Mignotte A Dubart D Beaupain P Leboulch M Romana C Chabret P Charnay T Papayannopoulou M Goossens 《The Journal of biological chemistry》1989,264(17):10186-10192