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Background: Although childhood sexual and/or physical abuse (CSA/CPA) is known to have severe psychopathological consequences, there is little evidence on psychotherapeutic interventions for adolescents and young adults suffering from post-traumatic stress disorder (PTSD). Equally sparse are data on moderators of treatment response on PTSD-related epigenetic changes, health care costs and loss of productivity, alterations in cognitive processing, and on how successful interventions affect all of these factors. Early treatment may prevent later (co)morbidity. In this paper, we present a study protocol for the evaluation of a newly developed psychotherapeutic manual for PTSD after CSA/CPA in adolescents and young adults – the Developmentally Adapted Cognitive Processing Therapy (D-CPT).
Methods/design: In a multicenter randomized controlled trial (RCT) D-CPT is compared to treatment as usual (TAU). A sample of 90 adolescent outpatients aged 14 to 21 years will be randomized to one of these conditions. Four assessments will be carried out at baseline, at end of treatment, and 3 and 6 months after end of therapy. Each time, patients will be assessed via clinical interviews and a wide range of questionnaires. In addition to PTSD symptoms and comorbidities, we will evaluate moderators of treatment response, epigenetic profiles, direct and indirect costs of this disorder, and neurophysiological processing of threat cues in PTSD and their respective changes in the course of these two treatments (D-CPT and TAU).
Discussion: The study will provide new insights in the understudied field of PTSD in adolescents and young adults. A newly developed intervention will be evaluated in this therapeutically underserved population. Results will provide data on treatment efficacy, direct and indirect treatment costs, as well as on associations of treatment outcome and PTSD intensity both to epigenetic profiles and to the neurobiological processing of threat cues. Besides, they will help to learn more about the psychopathology and possible new objective correlates of PTSD.
Trial registration: Germanctr.de identifier: DRKS00004787.
Dendritic cells (DCs) are the cutting edge in innate and adaptive immunity. The major functions of these antigen-presenting cells are the capture, endosomal processing and presentation of antigens, providing them an exclusive ability to provoke adaptive immune responses and to induce and control tolerance. Immature DCs capture and process antigens, migrate towards secondary lymphoid organs where they present antigens to naive T cells in a well-synchronized sequence of procedures referred to as maturation. Indeed, recent research indicated that sphingolipids are modulators of essential steps in DC homeostasis. It has been recognized that sphingolipids not only modulate the development of DC subtypes from precursor cells but also influence functional activities of DCs such as antigen capture, and cytokine profiling. Thus, it is not astonishing that sphingolipids and sphingolipid metabolism play a substantial role in inflammatory diseases that are modulated by DCs. Here we highlight the function of sphingosine 1-phosphate (S1P) on DC homeostasis and the role of S1P and S1P metabolism in inflammatory diseases.
Myocardial infarction (MI) induces a complex inflammatory immune response, followed by the remodelling of the heart muscle and scar formation. The rapid regeneration of the blood vessel network system by the attraction of hematopoietic stem cells is beneficial for heart function. Despite the important role of chemokines in these processes, their use in clinical practice has so far been limited by their limited availability over a long time-span in vivo. Here, a method is presented to increase physiological availability of chemokines at the site of injury over a defined time-span and simultaneously control their release using biodegradable hydrogels. Two different biodegradable hydrogels were implemented, a fast degradable hydrogel (FDH) for delivering Met-CCL5 over 24 hrs and a slow degradable hydrogel (SDH) for a gradual release of protease-resistant CXCL12 (S4V) over 4 weeks. We demonstrate that the time-controlled release using Met-CCL5-FDH and CXCL12 (S4V)-SDH suppressed initial neutrophil infiltration, promoted neovascularization and reduced apoptosis in the infarcted myocardium. Thus, we were able to significantly preserve the cardiac function after MI. This study demonstrates that time-controlled, biopolymer-mediated delivery of chemokines represents a novel and feasible strategy to support the endogenous reparatory mechanisms after MI and may compliment cell-based therapies.
Focus on quantum efficiency
(2014)
Technologies which convert light into energy, and vice versa, rely on complex, microscopic transport processes in the condensed phase, which obey the laws of quantum mechanics, but hitherto lack systematic analysis and modeling. Given our much improved understanding of multicomponent, disordered, highly structured, open quantum systems, this ‘focus on’ collection collects cuttingedge research on theoretical and experimental aspects of quantum transport in truly complex systems as defined, e.g., by the macromolecular functional complexes at the heart of photosynthesis, by organic quantum wires, or even photovoltaic devices. To what extent microscopic quantum coherence effects can (be made to) impact on macroscopic transport behavior is an equally challenging and controversial question, and this "focus on" collection provides a setting for the present state of affairs, as well as for the "quantum opportunities" on the horizon.
This paper deals with the control exerted by the mitochondrial translocator FLX1, which catalyzes the movement of the redox cofactor FAD across the mitochondrial membrane, on the efficiency of ATP production, ROS homeostasis, and lifespan of S. cerevisiae. The deletion of the FLX1 gene resulted in respiration-deficient and small-colony phenotype accompanied by a significant ATP shortage and ROS unbalance in glycerol-grown cells. Moreover, the flx1Δ strain showed H2O2 hypersensitivity and decreased lifespan. The impaired biochemical phenotype found in the flx1Δ strain might be justified by an altered expression of the flavoprotein subunit of succinate dehydrogenase, a key enzyme in bioenergetics and cell regulation. A search for possible cis-acting consensus motifs in the regulatory region upstream SDH1-ORF revealed a dozen of upstream motifs that might respond to induced metabolic changes by altering the expression of Flx1p. Among these motifs, two are present in the regulatory region of genes encoding proteins involved in flavin homeostasis. This is the first evidence that the mitochondrial flavin cofactor status is involved in controlling the lifespan of yeasts, maybe by changing the cellular succinate level. This is not the only case in which the homeostasis of redox cofactors underlies complex phenotypical behaviours, as lifespan in yeasts.
Background: The phagocytic enzyme myeloperoxidase (MPO) acts as a front-line defender against microorganisms. However, increased MPO levels have been found to be associated with complex and calcified atherosclerotic lesions and incident cardiovascular disease. Therefore, this study aimed to investigate a predictive role of MPO, a biomarker of inflammation and oxidative stress, for total and cardiovascular mortality in patients referred to coronary angiography.
Methods and results: MPO plasma concentrations along with eight MPO polymorphisms were determined in 3036 participants of the Ludwigshafen Risk and Cardiovascular Health study (median follow-up 7.75 years). MPO concentrations were positively associated with age, diabetes, smoking, markers of systemic inflammation (interleukin-6, fibrinogen, C-reactive protein, serum amyloid A) and vascular damage (vascular cellular adhesion molecule-1 and intercellular adhesion molecule-1) but negatively associated with HDL-cholesterol and apolipoprotein A-I. After adjustment for cardiovascular risk factors MPO concentrations in the highest versus the lowest quartile were associated with a 1.34-fold risk (95% CI: 1.09–1.67) for total mortality. In the adjusted model the hazard ratio for cardiovascular mortality in the highest MPO quartile was 1.42 (95% CI: 1.07–1.88). Five MPO polymorphisms were positively associated with MPO concentrations but not with mortality. Using Mendelian randomization, we did not obtain evidence for a causal association of MPO with either total or cardiovascular mortality.
Conclusions: MPO concentrations but not genetic variants at the MPO locus are independently associated with risk for total and cardiovascular mortality in coronary artery disease patients.
Here we present a formal description of Biremis panamae Barka, Witkowski et Weisenborn sp. nov., which was isolated from the marine littoral environment of the Pacific Ocean coast of Panama. The description is based on morphology (light and electron microscopy) and the rbcL, psbC and SSU sequences of one clone of this species. The new species is included in Biremis due to its morphological features; i.e. two marginal rows of foramina, chambered striae, and girdle composed of numerous punctate copulae. The new species also possesses a striated valve face which is not seen in most known representatives of marine littoral Biremis species. In this study we also present the relationship of Biremis to other taxa using morphology, DNA sequence data and observations of auxosporulation. Our results based on these three sources point to an evolutionary relationship between Biremis, Neidium and Scoliopleura. The unusual silicified incunabular caps present in them are known otherwise only in Muelleria, which is probably related to the Neidiaceae and Scoliotropidaceae. We also discuss the relationship between Biremis and the recently described Labellicula and Olifantiella.
Glioblastoma multiforme (GBM) is a deadly primary brain malignancy. Glioblastoma stem cells (GSC), which have the ability to self-renew and differentiate into tumor lineages, are believed to cause tumor recurrence due to their resistance to current therapies. A subset of GSCs is marked by cell surface expression of CD133, a glycosylated pentaspan transmembrane protein. The study of CD133-expressing GSCs has been limited by the relative paucity of genetic tools that specifically target them. Here, we present CD133-LV, a lentiviral vector presenting a single chain antibody against CD133 on its envelope, as a vehicle for the selective transduction of CD133-expressing GSCs. We show that CD133-LV selectively transduces CD133+ human GSCs in dose-dependent manner and that transduced cells maintain their stem-like properties. The transduction efficiency of CD133-LV is reduced by an antibody that recognizes the same epitope on CD133 as the viral envelope and by shRNA-mediated knockdown of CD133. Conversely, the rate of transduction by CD133-LV is augmented by overexpression of CD133 in primary human GBM cultures. CD133-LV selectively transduces CD133-expressing cells in intracranial human GBM xenografts in NOD.SCID mice, but spares normal mouse brain tissue, neurons derived from human embryonic stem cells and primary human astrocytes. Our findings indicate that CD133-LV represents a novel tool for the selective genetic manipulation of CD133-expressing GSCs, and can be used to answer important questions about how these cells contribute to tumor biology and therapy resistance.
MTO1-deficient mouse model mirrors the human phenotype showing complex I defect and cardiomyopathy
(2014)
Recently, mutations in the mitochondrial translation optimization factor 1 gene (MTO1) were identified as causative in children with hypertrophic cardiomyopathy, lactic acidosis and respiratory chain defect. Here, we describe an MTO1-deficient mouse model generated by gene trap mutagenesis that mirrors the human phenotype remarkably well. As in patients, the most prominent signs and symptoms were cardiovascular and included bradycardia and cardiomyopathy. In addition, the mutant mice showed a marked worsening of arrhythmias during induction and reversal of anaesthesia. The detailed morphological and biochemical workup of murine hearts indicated that the myocardial damage was due to complex I deficiency and mitochondrial dysfunction. In contrast, neurological examination was largely normal in Mto1-deficient mice. A translational consequence of this mouse model may be to caution against anaesthesia-related cardiac arrhythmias which may be fatal in patients.
Sleep is regulated in a time-of-day dependent manner and profits working memory. However, the impact of the circadian timing system as well as contributions of specific sleep properties to this beneficial effect remains largely unexplored. Moreover, it is unclear to which extent inter-individual differences in sleep-wake regulation depend on circadian phase and modulate the association between sleep and working memory. Here, sleep electroencephalography (EEG) was recorded during a 40-h multiple nap protocol, and working memory performance was assessed by the n-back task 10 times before and after each scheduled nap sleep episode. Twenty-four participants were genotyped regarding a functional polymorphism in adenosine deaminase (rs73598374, 12 G/A-, 12 G/G-allele carriers), previously associated with differences in sleep-wake regulation. Our results indicate that genotype-driven differences in sleep depend on circadian phase: heterozygous participants were awake longer and slept less at the end of the biological day, while they exhibited longer non rapid eye movement (NREM) sleep and slow wave sleep concomitant with reduced power between 8–16 Hz at the end of the biological night. Slow wave sleep and NREM sleep delta EEG activity covaried positively with overall working memory performance, independent of circadian phase and genotype. Moreover, REM sleep duration benefitted working memory particularly when occurring in the early morning hours and specifically in heterozygous individuals. Even though based on a small sample size and thus requiring replication, our results suggest genotype-dependent differences in circadian sleep regulation. They further indicate that REM sleep, being under strong circadian control, boosts working memory performance according to genotype in a time-of-day dependent manner. Finally, our data provide first evidence that slow wave sleep and NREM sleep delta activity, majorly regulated by sleep homeostatic mechanisms, is linked to working memory independent of the timing of the sleep episode within the 24-h cycle.
Escherichia coli α-hemolysin (HlyA) is a pore-forming protein of 110 kDa belonging to the family of RTX toxins. A hydrophobic region between the amino acid residues 238 and 410 in the N-terminal half of HlyA has previously been suggested to form hydrophobic and/or amphipathic α-helices and has been shown to be important for hemolytic activity and pore formation in biological and artificial membranes. The structure of the HlyA transmembrane channel is, however, largely unknown. For further investigation of the channel structure, we deleted in HlyA different stretches of amino acids that could form amphipathic β-strands according to secondary structure predictions (residues 71–110, 158–167, 180–203, and 264–286). These deletions resulted in HlyA mutants with strongly reduced hemolytic activity. Lipid bilayer measurements demonstrated that HlyAΔ71–110 and HlyAΔ264–286 formed channels with much smaller single-channel conductance than wildtype HlyA, whereas their channel-forming activity was virtually as high as that of the wildtype toxin. HlyAΔ158–167 and HlyAΔ180–203 were unable to form defined channels in lipid bilayers. Calculations based on the single-channel data indicated that the channels generated by HlyAΔ71–110 and HlyAΔ264–286 had a smaller size (diameter about 1.4 to 1.8 nm) than wildtype HlyA channels (diameter about 2.0 to 2.6 nm), suggesting that in these mutants part of the channel-forming domain was removed. Osmotic protection experiments with erythrocytes confirmed that HlyA, HlyAΔ71–110, and HlyAΔ264–286 form defined transmembrane pores and suggested channel diameters that largely agreed with those estimated from the single-channel data. Taken together, these results suggest that the channel-forming domain of HlyA might contain β-strands, possibly in addition to α-helical structures.
Previously we reported modulation of endothelial prostacyclin and interleukin-8 production, cyclooxygenase-2 expression and vasorelaxation by oleoyl-lysophosphatidylcholine (LPC 18:1). In the present study, we examined the impact of this LPC on nitric oxide (NO) bioavailability in vascular endothelial EA.hy926 cells. Basal NO formation in these cells was decreased by LPC 18:1. This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)-dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS). The LPC 18:1-induced ROS formation was attenuated by the superoxide scavenger Tiron, as well as by the pharmacological inhibitors of eNOS, NADPH oxidases, flavin-containing enzymes and superoxide dismutase (SOD). Intracellular ROS-formation was most prominent in mitochondria, less pronounced in cytosol and undetectable in endoplasmic reticulum. Importantly, Tiron completely prevented the LPC 18:1-induced decrease in NO bioavailability in EA.hy926 cells. The importance of the discovered findings for more in vivo like situations was analyzed by organ bath experiments in mouse aortic rings. LPC 18:1 attenuated the acetylcholine-induced, endothelium dependent vasorelaxation and massively decreased NO bioavailability. We conclude that LPC 18:1 induces eNOS uncoupling and unspecific superoxide production. This results in NO scavenging by ROS, a limited endothelial NO bioavailability and impaired vascular function.
Coevolution of viruses and their hosts represents a dynamic molecular battle between the immune system and viral factors that mediate immune evasion. After the abandonment of smallpox vaccination, cowpox virus infections are an emerging zoonotic health threat, especially for immunocompromised patients. Here we delineate the mechanistic basis of how cowpox viral CPXV012 interferes with MHC class I antigen processing. This type II membrane protein inhibits the coreTAP complex at the step after peptide binding and peptide-induced conformational change, in blocking ATP binding and hydrolysis. Distinct from other immune evasion mechanisms, TAP inhibition is mediated by a short ER-lumenal fragment of CPXV012, which results from a frameshift in the cowpox virus genome. Tethered to the ER membrane, this fragment mimics a high ER-lumenal peptide concentration, thus provoking a trans-inhibition of antigen translocation as supply for MHC I loading. These findings illuminate the evolution of viral immune modulators and the basis of a fine-balanced regulation of antigen processing.
Myotonic dystrophy type 1 (DM1) lacks non-invasive and easy to measure biomarkers, still largely relying on semi-quantitative tests for diagnostic and prognostic purposes. Muscle biopsies provide valuable data, but their use is limited by their invasiveness. microRNA (miRNAs) are small non-coding RNAs regulating gene expression that are also present in biological fluids and may serve as diseases biomarkers. Thus, we tested plasma miRNAs in the blood of 36 DM1 patients and 36 controls. First, a wide miRNA panel was profiled in a patient subset, followed by validation using all recruited subjects. We identified a signature of nine deregulated miRNAs in DM1 patients: eight miRNAs were increased (miR-133a, miR-193b, miR-191, miR-140-3p, miR-454, miR-574, miR-885-5p, miR-886-3p) and one (miR-27b) was decreased. Next, the levels of these miRNAs were used to calculate a "DM1-miRNAs score". We found that both miR-133a levels and DM1-miRNAs score discriminated DM1 from controls significantly and Receiver-Operator Characteristic curves displayed an area under the curve of 0.94 and 0.97, respectively. Interestingly, both miR-133a levels and DM1-miRNAs score displayed an inverse correlation with skeletal muscle strength and displayed higher values in more compromised patients. In conclusion, we identified a characteristic plasma miRNA signature of DM1. Although preliminary, this study indicates miRNAs as potential DM1 humoral biomarkers.
As part of a wider study of floodplain vegetation along the River Murray, we carried out a field survey in 1987–1988 involving collection of floristic and vegetation condition data from 335 sample plots (each 400 m2 in area), between Hume Dam and Lake Alexandrina (including the Edward-Wakool anabranch system). The floodplain vegetation is dominated by just two tree species, River Red Gum (Eucalyptus camaldulensis) and Black Box (Eucalyptus largiflorens), but the composition of the understorey shows much greater variation, both along the river and across the floodplain. A total of 499 plant species, subspecies and varieties were recorded from the survey plots, of which 316 (63%) were native and 183 (37%) were exotic. From analysis of the floristic data we identified 37 vegetation communities, not including the vegetation of permanent wetlands and cleared areas; 21 communities were distinguished in the River Red Gum zone, 12 communities in the Black Box zone, and 4 communities on rises within the floodplain. The main floristic division among the River Red Gum communities was between Riverine Plain/ Headwaters Zone communities of the upper Murray, and Mallee Zone communities of the lower Murray. Among the Black Box communities, the main floristic division was between inner floodplain communities and outer floodplain communities, with a further division between South Australian communities and New South Wales/Victorian communities. Major factors influencing the floristic patterns included flooding frequency/duration and soil salinity.
Eucalypt health declined steadily downstream and was poorest in the lower reaches of the river below the Darling Junction, where 60% of the trees were healthy, 18% unhealthy (at least 40% of the canopy dead) and 22% dead. By comparison, at the upper end of the river, above Tocumwal, 84% of the trees were healthy, 14% unhealthy and only 2% dead. Overall, the condition of Black Box trees (44% unhealthy or dead) was worse than the condition of River Red Gum trees (29% unhealthy or dead). Eucaypt regeneration was also poorest below the Darling Junction, with regenerants present in 77% of plots upstream of the Darling but only 35% of plots downstream. The findings of poor tree health and sparse regeneration below the Darling coincide with the most heavily regulated part of the Murray, where the reduction in flooding due to upstream storages and water extraction, mainly for irrigation, has been greatest. Black Box regeneration was much sparser overall than River Red Gum regeneration (regenerants present in 69% of River Red Gum plots but only 29% of Black Box plots). The poor condition of the Black Box trees, coupled with their poor regeneration, suggests that the long-term future of this species along the Murray, particularly below the Darling Junction, is tenuous, even though it is a dominant component of the vegetation.
The integrity of floodplain vegetation along the Murray has been severely compromised by weed invasion. Weeds were common throughout the survey area, but were most prevalent in the climatically wetter sections of the river, at both the downstream and upstream ends (below Mannum and above Tocumwal). The median number of exotic species per plot equalled or exceeded the number of native species in these sections of the river, whereas native species outnumbered exotic species in the other river sections. Communities of the River Red Gum zone and the rises were generally weedier than those of the Black Box zone. Exotic species strongly influenced the community classification. They were the dominant overstorey species in two communities (Salix species – willows) and outnumbered native species in the understorey of another eight communities. At the lower end of the river, below Mannum, the River Red Gums that originally fringed the river had been mostly replaced by dense thickets of the exotic Weeping Willow, Salix babylonica.
Other factors that have impacted on the floodplain vegetation at the plant community level have been river regulation and soil salinisation. Stabilization of water levels in the lower Murray by construction of a series of weirs and barrages has favoured the spread of some communities at the expense of others. The favoured communities, which are characterised by stands of Common Reed, Phragmites australis, along the water’s edge, appear to be artefacts of river regulation. Salinisation has resulted in death of eucalypts and replacement of eucalypt communities by shrub communities dominated by samphires, Tecticornia species. The samphire community characteristic of the most saline sites is one of the most species-poor communities on the Murray floodplain.
Logging along the Murray in New South Wales and Victoria has resulted in extensive replacement of old growth River Red Gum forests and woodlands by more even-aged stands of straight young trees. Following the recent conversion of many areas of State Forest along the Murray in both New South Wales and Victoria to National Park or Regional Park, and thus the cessation of logging in these areas, they should now revert gradually to mature forest and woodland.
This study is the first to describe broad scale floristic patterns in the floodplain vegetation of the Murray covering most of the length of the river. It also provides data on the vegetation condition in the 1980s, and provides a benchmark of conditions before the prolonged Millenium Drought in south-eastern Australia from 1997 to 2010. More recent surveys of vegetation condition have reported a severe decline in tree health during the drought. The results from our 1987–88 survey are important because they show that the deteriorating condition of the vegetation was already evident in the 1980s and although exacerbated by the subsequent drought, it is not just a consequence of that drought. The results are consistent with the conclusion that the primary cause of the decline has been river regulation and water extraction for irrigation. The rate of deterioration has increased rapidly since the 1980s because of the drought. There has been some improvement since the breaking of the drought, but the poor condition of the River Murray floodplain vegetation, an Australian icon, remains a major conservation and management issue. The impacts of climate change – higher temperatures and reduced rainfall – have compounded the problem and will continue to do so at an increasing rate. The results of the study support listing of the floodplain vegetation of the lower reaches of the river as a critically endangered ecological community.
The riparian rainforest on the streamside levees of the coastal floodplain of the Clarence River on the North Coast of New South Wales was cleared during the 1860s by small landholders seeking fertile land. Only three small remnants remain. Using a combination of historical species lists, corner trees from surveyors’ portion plans, habitat information and the NSW Scientific Committee’s (1999) determination for lowland rainforest on floodplain a conceptual model of the original distribution of rainforest suballiances on the levees of the Clarence River coastal floodplain is proposed.
Population size, and flowering and fruiting developmental stages in the Critically Endangered species Corunastylis sp. ‘Charmhaven’ (Family Orchidaceae, formerly included within genus Genoplesium), were investigated in the Warnervale-Charmhaven area over a three year period. Population size in 2012 was 11 plants, in 2013, 14 plants and in 2014 increased to 26 plants, with new plants appearing near the original plants. Proactive management, including mowing and erecting wire protective cages around groups of orchids was partly responsible for this increase in numbers because it prevented browsing by rabbits but only ten plants carried fruits to maturity in the 2014 season to produce seed. Despite an increase in numbers over a couple of years, a population of 26 individuals is very small and warrants maintaining the current conservation listing of Critically Endangered. The population began to flower between 15th and 29th February in 2012 and from 3rd to 14th March in 2013. However in 2014 flowering began on 11th February and extended to 19th March but it took until 17th June to reach the seed dispersal stage. 2014 involved two phases of flowering; whether climatic factors were responsible for this event is not known.
Acacia pendula, Weeping Myall, (family Fabaceae) is the most legislatively protected plant species in the New South Wales Hunter Valley. Under the NSW Threatened Species Conservation Act 1995 it is listed as an Endangered Population (in the Hunter Valley) and as a component of two Endangered Ecological Communities (one in the Hunter, one elsewhere in NSW); it is also listed as a Critically Endangered Ecological Community (in the Hunter Valley) on the Commonwealth Environment Protection and Biodiversity Conservation Act 1999 and listed as threatened in three other eastern Australian States.
To ascertain the likely original distribution of stands of Acacia pendula in the Hunter Valley, this paper examines the writings of early Australian explorers, herbarium and database records, and the species habitat attributes across NSW. None of the journals examined, including those of botanist/explorer Allan Cunningham (who originally collected Acacia pendula from the Lachlan River in 1817), Thomas Mitchell or Ludwig Leichhardt, make note of the species for the Hunter Valley. Several explorers do, however, record Acacia pendula regularly (>100 times) across other parts of NSW, Queensland, and South Australia.
Historical herbarium and database records show a paucity of records from the Hunter prior to the year 2000, after which a 37-fold increase in observations since 1951 is apparent. For the first 128 years of botanical exploration (1823 to 1951), there are no validated collections or records of Acacia pendula from the Hunter Valley. The single exception is a specimen collected by Cunningham from 1825 (lodged at Kew, UK), purported to be from ‘Hunters River’, but which is morphologically different to other collections of Acacia pendula from that time. There is some uncertainty over the origins of this specimen.
Analysis of habitats supporting Acacia pendula in NSW outside of the Hunter show them to differ significantly in geological age, soil type, rainfall and elevation from those in the Hunter.
Collectively, these findings provide a strong circumstantial case that Acacia pendula was absent from the Hunter at the time of European settlement; this has important implications for the conservation and management of Hunter stands. Rather than being a threatened species in the Hunter Valley, it is postulated that Acacia pendula has been intentionally and/or accidentally introduced to the region, and may now be imposing a new and emerging threat to the endangered grassy woodlands and forests there. There is now an urgent need for genetic studies to clarify the origins of the current Hunter Valley stands, and to define the taxonomic limits of Acacia pendula and its close relatives.
The availability of organelle genome sequences of bryophytes provides opportunity to mine this data. Therefore in this study microsatellites in chloroplast genome sequence of Pellia endiviifolia (Accession number: NC_019628), downloaded from the National Center for Biotechnology Information (NCBI) in fasta format, were identified. The sequence was mined with the help of MISA, a Perl script, to detect microsatellites. In total, 16 perfect microsatellites were identified in 120.546 kb sequence mined. An average length of 14.94 bp was calculated for mined microsatellites with a density of 1 SSR/7.09 kb. Depending on the repeat units, the length of microsatellites ranged from 12 to 18 bp. Tetranucleotides (7, 43.75%) were the most frequent repeat type, followed by mononucleotide (3, 18.75%) repeats. Dinucleotide, trinucleotide and pentanucleotide repeats were found with equal frequency (2, 12.5%). Interestingly, hexanucleotide repeats were completely absent in chloroplast genome of Pellia endiviifolia.
Coscinodon humilis was described by Milde from mica schist in the Passeiertal NE Merano (formerly southern Tyrolia in Austria, hence cited as Austria by Greven 1995. now Alto Adige in Italy). Limpricht (1890) regarded it as “verkümmerte Form von C. cribrosus”, and although Mönkemeyer (1927) still cited it, the species got forgotten by the time. Thus the species was no more mentioned by Corley et al (1981) in the European checklist and therefore no more included by Frey et al. (1995) in the German edition of the “Moos- und Farnpflanzen Europas”. Greven (1995) re-established the species in his treatment of Grimmia (and related genera) in Europe. Therefore Frey et al. (2006) included the species, which was, however, not keyed out. Finally Hill et al. (2006) listed it again in the new European checklist as a good species.