bluuebunny/crossref_metadata_2025_split huggingface dataset:
Large‐scale population dynamics, abundance–occupancy relationships and the scaling from local to regional population size
Authors: FRECKLETON R. P. , GILL J. A. , NOBLE D. , WATKINSON A. R. 
Published: March 2005

Summary

We explore the relationship between patch occupancy and local abundance in a general model for regional population dynamics. We vary colonization ability and key demographic and habitat characteristics in order to explore the effects on abundance–occupancy relationships.
In populations in which colonization rates are very high, new habitat is rapidly colonized and there is a simple asymptotic relationship between occupancy and abundance, assuming that habitat quality and abundance are linked.
If colonization rates are moderate to low, as in metapopulations, there is similarly a positive relationship between occupancy and abundance, but there is a minimum abundance below which the metapopulation becomes extinct.
These responses are modulated by the occurrence of Allee effects, demographic stochasticity or depensatory effects: when such effects are significant, the metapopulation rescue effect becomes important, and regional occupancy becomes more sensitive to changes in local density.
Finally, in populations in which colonization rates are very low, there is no relationship between occupancy and abundance.
Our results emphasize two aspects of large‐scale ecology as being key in generating positive abundance‐occupancy relationships: (i) a relationship between average habitat quality and the proportion of habitat that is habitable; and (ii) the nature of colonization. It is important to note that colonization is a function of dispersal, fecundity, and local processes such as Allee effects, as well as the availability and isolation of habitat patches.
When an abundance–occupancy relationship exists there is typically a non‐linear scaling from local to total population sizes at low population densities, and we discuss how this may be detected in real data, as well as its implications.
The pyruvate requirement of some members of the Mycobacterium tuberculosis complex is due to an inactive pyruvate kinase: implications for in vivo growth
Authors: Keating Lisa A. , Wheeler Paul R. , Mansoor Huma , Inwald Jacqueline K. , Dale James , Hewinson R. Glyn , Gordon Stephen V. 
Published: March 2005

SummaryThrough examination of one of the fundamental in vitro characteristics of Mycobacterium bovis– its requirement for pyruvate in glycerol medium – we have revealed a lesion in central metabolism that has profound implications for in vivo growth and nutrition. Not only is M. bovis unable to use glycerol as a sole carbon source but the lack of a functioning pyruvate kinase (PK) means that carbohydrates cannot be used to generate energy. This disruption in sugar catabolism is caused by a single nucleotide polymorphism in pykA, the gene which encodes PK, that substitutes glutamic acid residue 220 with an aspartic acid residue. Substitution of this highly conserved amino acid residue renders PK inactive and thus blocks the ATP generating roles of glycolysis and the pentose phosphate pathway. This mutation was found to occur in other members of the M. tuberculosis complex, namely M. microti and M. africanum. With carbohydrates unable to act as carbon sources, the importance of lipids and gluconeogenesis for growth in vivo becomes apparent. Complementation of M. bovis with the pykA gene from M. tuberculosis H37Rv restored growth on glycerol. Additionally, the presence of a functioning PK caused the colony morphology of the complemented strain to change from the characteristic dysgonic growth of M. bovis to eugonic growth, an appearance normally associated with M. tuberculosis. We also suggest that the glycerol‐soaked potato slices used for the derivation of the M. bovis bacillus Calmette and Guérin (BCG) vaccine strain selected for an M. bovis PK+ mutant, a finding that explains the alteration in colony morphology noted during the derivation of BCG. In summary, the disruption of a key step in glycolysis divides the M. tuberculosis complex into two groups with distinct carbon source utilization.
The HOG MAP kinase pathway is required for the induction of methylglyoxal‐responsive genes and determines methylglyoxal resistance in Saccharomyces cerevisiae
Authors: Aguilera Jaime , Rodríguez‐Vargas Sonia , Prieto Jose A. 
Published: March 2005

SummaryA sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG‐protective genes, including GPD1, GLO1 and GRE3. The response is partially dependent on the transcriptional factors Msn2p/Msn4p, but unrelated with the general stress response mechanism. Here, we show that the high‐osmolarity glycerol (HOG)‐pathway controls the genetic response to MG and determines the yeast growth capacity upon MG exposure. Strains lacking the MAPK Hog1p, the upstream component Ssk1p or the HOG‐dependent nuclear factor Msn1p, showed a reduction in the mRNA accumulation of MG‐responsive genes after MG addition. Moreover, hyperactivation of Hog1p by deletion of protein phosphatase PTP2 enhanced the response, while blocking the pathway by deletion of the MAPKK PBS2 had a negative effect. In addition, the activity of Hog1p affected the basal level of GPD1 mRNA under non‐inducing conditions. These effects had a great influence on MG resistance, as hog1Δ and other HOG‐pathway mutants with impaired MG‐specific expression displayed MG sensitivity, whereas those with enhanced expression exhibited MG resistance as compared with the wild‐type. However, MG does not trigger the overphosphorylation of Hog1p or its nuclear import in the parental strain. Moreover, dual phosphorylation of Hog1p appears to be dispensable in the triggering of the transcriptional response, although a phosphorylable form of Hog1p is fundamental for the transcriptional activity. Overall, our results suggest that the basal activity of the HOG‐pathway serves to amplify the expression of MG‐responsive genes under non‐inducing and inducing conditions, ensuring cell protection against this toxic glycolytic by‐product.
Cryo‐electron microscopy reveals native polymeric cell wall structure in Bacillus subtilis 168 and the existence of a periplasmic space
Authors: Matias Valério R. F. , Beveridge Terry J. 
Published: March 2005

SummaryUltrarapid freezing of bacteria (i.e. vitrification) results in optimal preservation of native structure. In this study, cryo‐transmission electron microscopy of frozen‐hydrated sections was used to gain insight into the organization of the Bacillus subtilis 168 cell envelope. A bipartite structure was seen above the plasma membrane consisting of a low‐density 22 nm region above which a higher‐density 33 nm region or outer wall zone (OWZ) resided. The interface between these two regions appeared to possess the most mass. In intact and in teichoic acid‐extracted wall fragments, only a single region was seen but the mass distribution varied from being dense on the inside to less dense on the outside (i.e. similar to the OWZ). In plasmolysed cells, the inner wall zone (IWZ)'s thickness expanded in size but the OWZ's thickness remained constant. As the IWZ expanded it became filled with plasma membrane vesicles indicating that the IWZ had little substance and was empty of the wall's polymeric network of peptidoglycan and teichoic acid. Together these results strongly suggest that the inner zone actually represents a periplasmic space confined between the plasma membrane and the wall matrix and that the OWZ is the peptidoglycan‐teichoic acid polymeric network of the wall.
Trypanosoma brucei MOB1 is required for accurate and efficient cytokinesis but not for exit from mitosis
Authors: Hammarton Tansy C. , Lillico Simon G. , Welburn Sue C. , Mottram Jeremy C. 
Published: March 2005

SummaryTwo MOB1 genes, MOB1‐A and MOB1‐B, were identified in Trypanosoma brucei. MOB1‐A of T. brucei was shown to form a complex with TbPK50, a functional homologue of the Schizosaccharomyces pombe protein kinase Orb6, and immune precipitated MOB1‐A exhibited histone H1 protein kinase activity. MOB1‐A and TbPK50 were also shown to bind p12cks1, a cyclin‐dependent kinase accessory protein. Immune fluorescence of epitope‐tagged MOB1‐A and MOB1‐B in bloodstream form trypanosomes showed they had a punctate distribution all through the cell cytoplasm and were excluded from the nucleus throughout the cell cycle. Using RNA interference (RNAi), MOB1 was shown to be essential in both bloodstream and procyclic life cycle stages. In the bloodstream form, RNAi of MOB1 resulted, after 8 h, in a significant increase in post‐mitotic cells, the majority of which had a visible cleavage furrow. This was followed by the appearance of cells with abnormal complements of nuclei and kinetoplasts, often with the number of nuclei exceeding the number of kinetoplasts. Thus, downregulation of MOB1 in the bloodstream form results in a delay in cytokinesis, and leads to a deregulation of the cell cycle, possibly through an inhibitory effect on kinetoplast replication. In contrast, downregulation of MOB1 in the procyclic form appears to impede the accuracy of cytokinesis, by allowing mispositioning of the cleavage furrow and inappropriate cytokinesis. Unlike its counterpart in budding yeast, T. brucei MOB1 does not appear to be required for mitotic exit.
Spontaneous and directed application of verbal learning strategies in bipolar disorder and obsessive‐compulsive disorder
Authors: Deckersbach Thilo , Savage Cary R , Dougherty Darin D , Bohne Antje , Loh Rebecca , Nierenberg Andrew , Sachs Gary , Rauch Scott L 
Published: March 2005

Objectives: Individuals with bipolar disorder exhibit neuropsychological impairments when they are euthymic (neither depressed nor manic). One of the most consistently reported cognitive problems in euthymic individuals with bipolar disorder is impairment in verbal episodic memory. Recent findings suggest that episodic memory difficulties in these individuals are attributable to difficulties using organizational strategies during encoding. The purpose of the present study was (i) to investigate whether difficulties using organizational strategies in bipolar disorder are due to a failure in spontaneously initiating verbal organization strategies or are due to difficulties implementing such strategies, and (ii) to compare the characteristics of verbal organizational impairment in bipolar disorder with those observed in individuals with obsessive–compulsive disorder (OCD).Methods: Study participants were 20 individuals with bipolar I disorder (BP‐I), 20 individuals with OCD, and 20 healthy control participants matched for age, gender, and education. Participants completed a verbal encoding paradigm that involved spontaneous and directed use of verbal organization strategies during encoding of word lists.Results: Compared with control subjects, both BP‐I and OCD participants showed impaired verbal organization in the spontaneous encoding condition. In the directed encoding condition, OCD patients organized the word lists as well as control participants whereas BP‐I participants exhibited lower verbal organization than both control and OCD participants. OCD and BP‐I participants’ free recall performance did not differ from that of control participants in the spontaneous encoding condition. In the directed encoding condition, BP‐I participants recalled fewer words than OCD or control participants.Conclusions: Episodic memory difficulties in OCD are associated with difficulties spontaneously initiating verbal organization strategies during encoding whereas the ability to implement verbal organization when instructed to do so is preserved. BP‐I participants, on the other hand, exhibit difficulties in both spontaneously initiating verbal organization strategies and in the ability to implement such strategies when instructed to do so.
An investigation of prepulse inhibition in pediatric bipolar disorder
Authors: Rich Brendan A , Vinton Deborah , Grillon Christian , Bhangoo Robinder K , Leibenluft Ellen 
Published: March 2005

Objectives:  Deficits in prepulse inhibition (PPI), a measure of sensorimotor gating, have been noted in psychopathologies including schizophrenia and adult bipolar disorder (BPD). Sensorimotor gating deficits may contribute to the emotional and behavioral dysregulation characteristic of pediatric BPD. The current study investigated possible PPI deficits in children with BPD.Methods:  Sixteen children with BPD (medicated, euthymic and non‐psychotic) were compared with 13 control subjects on the magnitude of startle habituation, startle‐alone response, and inhibition of startle following a 60 or 120‐ms prepulse.Results:  Both groups displayed startle inhibition by a prepulse, with no significant between‐group differences on the magnitude of inhibition after the 60‐ or 120‐ms prepulse. In addition, there were no between‐group differences on habituation or baseline startle response. PPI level was not significantly correlated with mood symptoms and did not differ based on comorbid attention deficit hyperactivity disorder.Conclusions:  A lack of PPI deficits in our pediatric bipolar sample contrasts with previous results in adult bipolar and schizophrenic samples. These negative results may reflect the fact that our sample was medicated and was neither acutely manic nor psychotic. Deficits in sensorimotor gating may not be implicated in the emotional and behavioral dysregulation in pediatric BPD.
Effects of Aβ1−42 fibrils and of the tetrapeptide Pr‐IIGL on the phosphorylation state of the τ‐protein and on the α7 nicotinic acetylcholine receptor in vitro
Authors: Lain Enzo , Penke Botond , Delacourte André , Gündisch Daniela , Schröder Hannsjörg , Witter Brigitte 
Published: March 2005

AbstractIn order to investigate the possible links connecting β‐amyloid (Aβ) accumulation, τ‐hyperphosphorylation and nicotinic receptor expression, rat embryonic primary hippocampal cultures were incubated with amyloidogenic peptides. Exposure to 0.5 µm fibrillar Aβ1−42 for 3 days caused retraction of dendrites, shrinkage of cell bodies and a decrease in the expression of microtubule‐associated proteins 2b (MAP2b), without affecting the total number of neurons and their viability. No impact on the τ‐phosphorylation sites Ser‐202, Thr231/Ser235, Ser262 and Ser396/Ser404 was found. The total number of homomeric α7‐nicotinic receptors (α7‐nAChRs) and their affinity for [125I]α‐bungarotoxin remained unaltered. Upon incubation with the putatively protective tetrapeptide propionyl–isoleucine–isoleucine–glycine–leucine (Pr‐IIGL), an analogue of the region [31–34] of Aβ, cell bodies were swollen in the region of the apical dendrite. These morphological alterations, different from those elicited by Aβ1−42, did not involve MAP2 expression changes. In contrast to Aβ1−42, Pr‐IIGL caused a massive hyperphosphorylation of the τ‐protein at Ser‐202 and at Ser396/Ser404. The total number of homomeric α7‐nAChRs and their affinity for [125I]α‐bungarotoxin were unaffected. In conclusion, the present results show a toxic effect of Aβ1−42 on the cytoskeletal structure at concentrations normally present in the brains of Alzheimer's disease patients, but raise some doubts about the role of Aβ1−42 fibrils as a direct trigger of τ‐hyperphosphorylation. The tetrapeptide Pr‐IIGL cannot be considered protective with regard to cell morphology. Although it prevents the Aβ1−42‐induced retraction of dendrites, it exhibits other toxic properties. The homomeric α7‐nAChRs were not affected either by Aβ1−42 incubation or by Pr‐IIGL‐induced τ‐hyperphosphorylation.
REM sleep: a sensitive index of fear conditioning in rats
Authors: Jha Sushil K. , Brennan Francis X. , Pawlyk Aaron C. , Ross Richard J. , Morrison Adrian R. 
Published: March 2005

AbstractTo examine the influence of conditioned fear stimuli on sleep‐wake states, we recorded sleep in Sprague–Dawley rats after exposure to tones previously paired with footshock. After habituation to a recording chamber and the recording procedure, a baseline sleep recording was obtained the next day. One day later, experimental animals were exposed to shock training designed to induce conditioned fear (FC), consisting of five tone‐footshock pairings. The 5‐s tones (conditioned stimuli; CS) co‐terminated with 1‐s footshocks (unconditioned stimuli; US). The next day sleep was recorded for 4 h in the recording chamber after presentation of five CSs alone. Sleep efficiency (total sleep time/recording period) and REM sleep (REM) and non‐REM (NREM) measures were determined. While sleep efficiency was not significantly changed after CS presentation, the percentage of total sleep time spent in REM (REM percentage) was reduced in the FC animals. The reduction in REM percentage in the FC animals was due to a decrease in the number of REM bouts. In a separate experiment, we repeated the procedures, except the tones and shocks were presented in an explicitly unpaired (UP) fashion. The next day, presentation of the tones increased REM percentage in the UP group. Results are discussed in terms of the decreases in REM as a response to conditioned fear, and the relevance of these findings to the sleep changes seen in post‐traumatic stress disorder (PTSD).
Activation of nuclear factor‐κB signaling pathway by interleukin‐1 after hypoxia/ischemia in neonatal rat hippocampus and cortex
Authors: Hu Xiaoming , Nesic‐Taylor Olivera , Qiu Jingxin , Rea Harriett C. , Fabian Roderick , Rassin David K. , Perez‐Polo J. Regino 
Published: March 2005

AbstractPerinatal hypoxia/ischemia (HI) is a common cause of neurological deficits in children. Interleukin‐1 (IL‐1) activity has been implicated in HI‐induced brain damage. However, the mechanisms underlying its action in HI have not been characterized. We used a 7‐day‐old rat model to elucidate the role of nuclear factor‐κB (NF‐κB) activation in HI stimulation of IL‐1 signaling. HI was induced by permanent ligation of the left carotid artery followed by 90 min of hypoxia (7.8% O2). Using ELISA assays, we observed increased cell death and caspase 3 activity in hippocampus and cortex 3, 6, 12, 24 and 48 h post‐HI. IL‐1β protein expression increased, beginning at 3 h after HI and lasting until 24 h post‐HI in hippocampus and 12 h post‐HI in cortex. Intracerebroventricular injection of 2µg IL‐1 receptor antagonist (IL‐1Ra) 2 h after HI significantly reduced cell death and caspase 3 activity. Electrophoretic mobility shift assay analyses of hippocampus and cortex after HI for NF‐κB activity showed increased p65/p50 DNA‐binding activity at 24 h post‐HI. Western blot analyses showed significant nuclear translocation of p65. Protein expression levels of two known inflammatory agents, inducible nitric oxide synthase and cycloxygenase 2, known to be transcriptionally regulated by NF‐κB, also increased at 24 h after HI. All these HI‐induced changes were reversed by IL‐1Ra blockade of IL‐1 signaling, consistent with IL‐1 triggering of inflammatory apoptotic outcomes via NF‐κB transcriptional activation. The observed increase in cytoplasmic phosphorylated inhibitor κBα (IκBα) and nuclear translocation of Bcl‐3 24 h after HI was also significantly attenuated by IL‐1Ra blockade, suggesting that HI‐induced IL‐1 activation of NF‐κB is via both the degradation of IκBα and the nuclear translocation of Bcl‐3.
M opsin phosphorylation in intact mammalian retinas
Authors: Liu Peng , Osawa Shoji , Weiss Ellen R. 
Published: March 2005

AbstractThe deactivation of visual pigments involved in phototransduction is critical for recovering sensitivity after exposure to light in rods and cones of the vertebrate retina. In rods, phosphorylation of rhodopsin by rhodopsin kinase (GRK1) and the subsequent binding of visual arrestin completely terminates phototransduction. Although signal termination in cones is predicted to occur via a similar mechanism as in rods, there may be differences due to the expression of related but distinct gene products. While rods only express GRK1, cones in some species express only GRK1 or GRK7 and others express both GRKs. In the mouse, cone opsin is phosphorylated by GRK1, but this has not been demonstrated in mammals that express GRK7 in cones. We compared cone opsin phosphorylation in intact retinas from the 13‐lined ground squirrel (GS) and pig, cone‐ and rod‐dominant mammals, respectively, which both express GRK7. M opsin phosphorylation increased during continuous exposure to light, then declined between 3 and 6 min. In contrast, rhodopsin phosphorylation continued to increase during this time period. In GS retina homogenates, anti‐GS GRK7 antibody blocked M opsin phosphorylation by 73%. In pig retina homogenates, only 20% inhibition was observed, possibly due to phosphorylation by GRK1 released from rods during homogenization. Our results suggest that GRK7 phosphorylates M opsin in both of these mammals. Using an in vitro GTPγS binding assay, we also found that the ability of recombinant M opsin to activate Gt was greatly reduced by phosphorylation. Therefore, phosphorylation may participate directly in the termination of phototransduction in cones by decreasing the activity of M opsin.
THE DISTRIBUTION OF WEALTH IN CANADA
Authors: Oja Gail 
Published: March 2005

For estimates of the wealth distribution Canada depends on household surveys taken at 6–7 year intervals. The latest data from this source refer to household balance sheets in the spring of 1977. A comparison with 1970 shows that there is little change in the composition of wealth held by households but that inequality of the wealth distribution has been somewhat reduced. Wealth data by age of family head is presented in order to describe more fully the wealth distribution and composition in Canada.Weaknesses in the data are discussed as well as the difficulties of making appropriate adjustments to the data at the micro record level. For policy evaluation and formulation purposes the lack of comprehensive estimates inclusive of pension wealth as well as the small sample size (12,700 usable records) have been perceived as greater obstacles to utilizing the data than the underestimate in aggregate assets and debts which affects more the higher than the middle and lower ranges of the wealth distribution.
DETERMINANTS OF BANK HOLDING COMPANY DEBT RATINGS
Authors: Billingley Randall S. , Fraser Donald R. 
Published: March 2005

AbstractThis paper reports on the construction of a multiple discriminant analysis model which explains the specific ratings assigned by Standard and Poor's Corporation to bank holding company (BHC) capital notes and debentures. It thus investigats the ratings of debt securities issued by banking organizations, an area largely ignored in bond rating research to date. Improving on the methodology of current research concerning BHC bond ratings, the model is 78.5 percent accurate in initially classifying the top three rating categories—AAA, AA, and A. Lachenbruch validation finds the model to be 64.6 percent accurate. Size, variability of net income, the economic environment of the issuing BHC, and the amount and composition of total capital appear to be the principal variables allowing successful discrimination among the debet issue ratings.
AN ANALYTICAL MODEL OF THE RELATIONSHIP BETWEEN MATURITY AND BONDS RISK DIFFERENTIALS
Authors: Chiang Raymond , Kolb Robert W. 
Published: March 2005

ABSTRACTThis paper extends previous analyses of bond risk differentials by relaxing the key assumption of a constant probability of firm survival. Under the less restrictive assumption that firm income is stationary and independent over time, it is shown that risk differential clearly varies with maturity even with a flat term structure. Because the payoff possibilities of multi‐period bonds are interdependent even though income in each period is independent, risk differentials must depend on maturity, even if term structure is flat. This conclusion is more compatible with empirical findings than were conclusions of previous analyses.