bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ecological effects of perturbation by drought in flowing waters
Authors: Lake P. S. 
Published: June 2003

SUMMARY

Knowledge of the ecology of droughts in flowing waters is scattered and fragmentary, with much of the available information being gathered opportunistically. Studies on intermittent and arid‐zone streams have provided most of the information.
Drought in streams may be viewed as a disturbance in which water inflow, river flow and water availability fall to extremely low levels for extended periods of time. As an ecological perturbation, there is the disturbance of drought and the responses of the biota to the drought.
Droughts can either be periodic, seasonal or supra‐seasonal events. The types of disturbance for seasonal droughts are presses and for supra‐seasonal droughts, ramps.
In droughts, hydrological connectivity is disrupted. Such disruption range from flow reduction to complete loss of surface water and connectivity. The longitudinal patterns along streams as to where flow ceases and drying up occurs differs between streams. Three patterns are outlined: ‘downstream drying’, ‘headwater drying’ and ‘mid‐reach drying’.
There are both direct and indirect effects of drought on stream ecosystems. Marked direct effects include loss of water, loss of habitat for aquatic organisms and loss of stream connectivity. Indirect effects include the deterioration of water quality, alteration of food resources, and changes in the strength and structure of interspecific interactions.
Droughts have marked effects on the densities and size‐ or age‐structure of populations, on community composition and diversity, and on ecosystem processes.
Organisms can resist the effects of drought by the use of refugia. Survival in refugia may strongly influence the capacity of the biota to recover from droughts once they break.
Recovery by biota varies markedly between seasonal and supra‐seasonal droughts. Faunal recovery from seasonal droughts follows predictable sequences, whilst recovery from supra‐seasonal droughts varies from one case to another and may be marked by dense populations of transient species and the depletion of biota that normally occur in the streams.
The restoration of streams must include the provision of drought refugia and the inclusion of drought in the long‐term flow regime.
Drought in an evolutionary context: molecular variability in Flannelmouth Sucker (Catostomus latipinnis) from the Colorado River Basin of western North America
Authors: Douglas Marlis R. , Brunner Patrick C. , Douglas Michael E. 
Published: June 2003

Summary 1. Fishes can often rebound numerically and distributionally from short‐term (i.e. seasonal) drought, yet their capacity to recover from decades or centuries of drought is less apparent. An exceedingly warm and dry period swept the intermontane west of North America ca. 7500 years BP, concomitant with an abrupt extinction of >35 mammal species. Were larger fishes in mainstem rivers also impacted by this drought?2. The Colorado River Basin encompasses seven states in western North America and drains 600 000 km2. Its endemic mainstem fish community is ancient (i.e. Miocene) but depauperate.3. We evaluated one widely distributed candidate species (flannelmouth sucker, Catostomus latipinnis) for basin‐wide genetic and geographic structure at three fast‐evolving mitochondrial (mt) DNA genes, ND2 with 589 bp and ATPase 8 and 6 with 642 bp. It is hypothesized that a concomitant signature would be present in the mtDNA of this species, if indeed it had been seriously bottlenecked by post‐Pleistocene drought. A total of 352 individuals were sequenced from 24 populations (4–40 individuals/population; average of 14.7).4. Only 49 unique haplotypes were found, 53% of which represented single individuals. Haplotype diversity was high (0.905 ± 0.007) whereas nucleotide diversity was low (0.002 ± 0.000).5. A significant and positive geographical cline (P < 0.001) in nucleotide diversity was observed as sampling locations progressed upstream from southwest to northeast. These results divided the Colorado River Basin into three reaches: the lower reach with six populations and 83 individuals; the upper reach with seven populations and 83 individuals; and the middle reach with 11 populations and 186 individuals. An analysis of molecular variance (amova) revealed that 81.5% of the total genetic variation was within populations, 16% among populations within reaches and 2.5% among reaches. Only the last was significant. Populations from the three reaches diverged from one another by 3400–11 000 years BP. Haplotype distribution suggested populations in the upper Colorado River are expanding.6. The lack of genetic variation and recent coalescence of lineages in C. latipinnis are unusual given its fossil history, broad geographical sampling, the rapid rate of mtDNA evolution and the number (and evolutionary rate) of the genes examined. The most parsimonious explanation for these data is a rapid expansion following a recent period of low effective population size at the end of the Pleistocene.7. The intense drought is suggested at the end of the Pleistocene (late‐to‐mid‐Holocene), severely impacted not only large mammals but also larger fishes in western North American rivers. These perspectives have important implications for management of endangered and threatened species in this region.
Droughts and anti‐droughts: the low flow hydrology of Australian rivers
Authors: McMahon T. A. , Finlayson B. L. 
Published: June 2003

Summary1. Droughts are not easily defined other than by culturally driven judgements about the extent and nature of impact. Natural ecosystems are adapted to the magnitude and frequency of dry periods and these are instrumental in controlling the long term functioning of these systems.2. In unregulated rivers, low flows are derived from water in long‐term storage in the catchment, commonly as shallow groundwater. Four types of low flow sequences are evident for representative rivers from each of the seven flow regime zones in Australia and an arid zone stream: perennial streams with low annual flow variability that have seasonal low flows but do not cease to flow; perennial streams with high annual variability that cease to flow in extreme years; ephemeral streams that regularly cease to flow in the dry season; and arid zone streams with long and erratic periods of no flow.3. Although Australian rivers record runs of consecutive years of low flows longer than would be expected theoretically, the departures from the expected are not statistically significant. Trends and quasi‐cycles in sequences of low‐flow years are observed over decadal time scales.4. Examples of the effects of river regulation on low flows in southern Australia indicate that, while in detail the impacts of regulation vary, in general regulation mitigates the severity of low flows.5. It is our contention that the indigenous biota of Australian rivers are adapted to the naturally occurring low flow conditions and that, while there is considerable scientific interest in the effects of climate change on stream ecology, such studies have little practical relevance for the management of indigenous biota in unregulated rivers.6. The changes brought about by the regulation of rivers are much more rapid and dramatic than those which might occur as a result of climate change and it is possible to develop management procedures to mitigate them. In regulated rivers, the real problem may be ‘anti‐droughts’– the removal of significant natural low‐flow events from the flow pattern.
Characterization of extrathymic CD8αβ T cells in the liver and intestine in TAP‐1 deficient mice
Authors: Tsukada Chika , Miyaji Chikako , Kawamura Hiroki , Miyakawa Ryoko , Yokoyama Hisashi , Ishimoto Yuiko , Miyazawa Shinobu , Watanabe Hisami , Abo Toru 
Published: June 2003

SummaryTAP‐1 deficient (−/−) mice cannot transport MHC class I antigens onto the cell surface, which results in failure of the generation of CD8+ T cells in the thymus. In a series of recent studies, it has been proposed that extrathymic T cells are generated in the liver and at other extrathymic sites (e.g. the intestine). It was therefore investigated whether CD8+ extrathymic T cells require an interaction with MHC class I antigens for their differentiation in TAP‐1(−/−) mice. Although CD8+ thymically derived T cells were confirmed to be absent in the spleen as well as in the thymus, CD8αβ+ T cells were abundant in the livers and intestines of TAP‐1(−/−) mice. These CD8+ T cells expanded in the liver as a function of age and were mainly confined to a NK1·1−CD3int population which is known to be truly of extrathymic origin. Hepatic lymphocytes, which contained CD8+ T cells and which were isolated from TAP‐1(−/−) mice (H‐2b), responded to neither mutated MHC class I antigens (bm1) nor allogeneic MHC class I antigens (H‐2d) in in vitro mixed lymphocyte cultures. However, the results from repeated in vivo stimulations with alloantigens (H‐2d) were interesting. Allogeneic cytotoxicity was induced in liver lymphocytes in TAP‐1(−/−) mice, although the magnitude of cytotoxicity was lower than that of liver lymphocytes in immunized B6 mice. All allogeneic cytotoxicity disappeared with the elimination of CD8+ cells in TAP‐1(−/−) mice. These results suggest that the generation and function of CD8+ extrathymic T cells are independent of the existence of the MHC class I antigens of the mouse but have a limited allorecognition ability.
Evidence for the immunosuppressive role of nicotine on human dendritic cell functions
Authors: Nouri‐Shirazi Mahyar , Guinet Elisabeth 
Published: June 2003

SummaryNicotine alters a wide range of immunological functions, including innate and adaptive immune responses. To date, no studies have been reported showing the immunoregulatory effects of nicotine on dendritic cells (DCs), which are critical cells for initiation of cell‐mediated immunity against infection and neoplastic diseases. In this work, we report that, in a nicotinic environment, monocyte‐derived DCs manifest lower endocytic and phagocytic activities. Interestingly, although immature DCs undergo maturation in response to bacterial antigen lipopolysaccharide, they produce decreased levels of pro‐inflammatory cytokines, notably interleukin‐12, and reveal a reduced ability to stimulate antigen‐presenting cell‐dependent T‐cell responses. Importantly, the reduction in T‐cell responses is associated with a diminished ability of DCs to induce differentiation and expansion of type 1 T cells, as evidenced by a decreased frequency of interferon‐γ‐producing effector cells. These results strongly suggest that nicotine can exert its immunosuppressive effects on immune surveillance through functional impairment of the DC system.
Differential T‐cell activation by B7‐1 expression
Authors: Li Wei , Rosenzweig Anthony , Huber Brigitte T. 
Published: June 2003

SummaryT‐cell receptor‐mediated T‐cell activation requires cosimulation signal, which can be provided by B7‐1 molecule. Our previous study demonstrated that the coexpression of a covalent peptide/major histocompatibility complex class II molecule complex and costimulatory molecule B7‐1 by recombinant adenovirus leads to synergy in peptide‐specific T‐cell activation. However, the viral antigen‐specific T‐cell activation is not enhanced by B7‐1 expressed by the adenovirus. To verify the differential T cell activation by B7‐1 and investigate its underlying mechanisms, we constructed an adenovirus coexpressing a covalent complex of hen egg lysozyme peptide/I‐Ak (HEL46–61/I‐Ak) and B7‐1 in the present study. In vivo studies revealed that HEL46–61‐specific T‐cell response, but not viral antigen‐specific T‐cell response, was enhanced by B7‐1 expression mediated by the adenovirus, suggesting that exogenous B7‐1 expression may regulate T‐cell response to these two different antigens through distinct mechanisms. Furthermore, our results revealed that antigen‐presenting cells were unsusceptible to adenovirus infection in vivo. Based on these findings, the possible mechanism of differential B7‐1 costimulation on peptide‐specific and viral antigen‐specific T‐cell activation is discussed.
Protein kinase C is involved in 2B4 (CD244)‐mediated cytotoxicity and AP‐1 activation in natural killer cells
Authors: Chuang Samuel S. , Lee Jae‐Kyung , Mathew Porunelloor A. 
Published: June 2003

Summary2B4 (CD244) is a member of the CD2 subset of the immunoglobulin superfamily and functions as a triggering molecule on natural killer (NK) cells. Previously, we have found that 2B4‐mediated activation of NK cells involves complex interactions involving LAT, Ras, Raf, ERK and p38 and that cytolytic function and cytokine production may be regulated by distinct pathways. Here we assessed the role of protein kinase C (PKC) in 2B4‐mediated cytotoxicity of YT cells, a human NK cell line. Our data indicate that PKC‐δ is activated upon stimulation with monoclonal antibody against 2B4. Treatment with the PKC inhibitor, bisindolylmaleimide I (Gö6850), of YT cells or YT cells depleted of Ca2+‐dependent isoforms of PKC prior to 2B4 stimulation, resulted in inhibition of natural cytotoxicity and redirected antibody‐dependent cellular cytotoxicity. However, inhibition of PKC failed to block 2B4 stimulation of interferon‐γ secretion as opposed to pretreatment with LY294002, a phosphoinositide 3‐kinase inhibitor. We also examined the effect of phorbol 12‐myristate 13‐acetate (PMA) induction on 2B4 gene transcription. PMA induction resulted in a more than two‐fold increase of 2B4 transcription. However, when we introduced a three‐base substitution mutation to disrupt the activator protein‐1 binding site at (−106 to −100) in the 2B4 promoter, we found complete loss of transcriptional activity, including the two‐fold increase due to PMA induction of PKC. The present study indicated that PKC may play an important role in 2B4 signalling and activator protein‐1 activation.
The role of interferon‐γ, nitric oxide and lipopolysaccharide in intestinal graft‐versus‐host disease developing in F1‐hybrid mice
Authors: Ellison Cynthia A. , Natuik Shannon A. , Mcintosh Alan R. , Scully Sheila A. , Danilenko Dimitry M. , Gartner John G. 
Published: June 2003

Summary(C57BL/6 × DBA/2)F1‐hybrid mice injected with lymphoid cells from wild‐type, C57BL/6 donors develop acute, lethal graft‐versus‐host disease (GVHD) in which the intestine is a major target. In its destructive phase intestinal GVHD is characterized by apoptosis of intestinal crypt epithelial cells and the development of endotoxaemia. Injection of as little as 10 μg endotoxin is lethal in mice with acute GVHD, and associated with the release of large amounts of tumour necrosis factor‐α (TNF‐α) into the serum. To explore the role of interferon‐γ (IFN‐γ) in the pathogenesis of intestinal GVHD we used IFN‐γ gene knockout (gko) mice as donors. Recipients of grafts from these donors did not develop intestinal GVHD and, unlike recipients of wild‐type grafts, did not die when injected with lipopolysaccharide (LPS). We also found that injection 10 μg LPS into recipients of wild‐type grafts induced apoptosis of intestinal epithelial crypt cells and was associated with a burst of nitric oxide production in the intestine. Administration of Nωnitro l‐arginine methyl ester blocked this response. In contrast, LPS did not induce either intestinal epithelial cell apoptosis or increased nitric oxide production in recipients of IFN‐γ gko grafts. These findings indicate that donor‐derived IFN‐γ is instrumental for the development of intestinal GVHD. In a previous study we showed that recipients of IFN‐γ gko grafts develop high levels of LPS‐induced TNF‐α release. When our current data are viewed in the context of this observation, they suggest that intestinal epithelial cell apoptosis in the parent→F1‐hybrid model of acute GVHD is mediated primarily by nitric oxide rather than TNF‐α, and that this depends on donor‐derived IFN‐γ.
Dendritic cell maturation enhances CD8+ T‐cell responses to exogenous antigen via a proteasome‐independent mechanism of major histocompatibility complex class I loading
Authors: Robson Neil C. , Beacock‐Sharp Helen , Donachie Anne M. , Mowat Allan McI. 
Published: June 2003

SummaryImmune stimulating complexes (ISCOMS) containing the saponin adjuvant Quil A are vaccine adjuvants that induce a wide range of immune responses in vivo, including strong class I major histocompatibility complex (MHC) ‐restricted cytotoxic T‐lymphocyte activity. However, the antigen‐presenting cell responsible for the induction of these responses has not been characterized. Here we have investigated the role of dendritic cells (DC) in the priming of antigen‐specific CD8+ T cells in vitro by ISCOMS containing ovalbumin. Resting bone marrow DC pulsed with ovalbumin ISCOMS efficiently prime resting CD8+ T cells through a mechanism that is transporter associated with antigen processing (TAP) dependent, but independent of CD40 ligation and CD4+ T‐cell help. Lipopolysaccharide‐induced maturation of DC markedly enhances their ability to prime CD8+ T cells through a mechanism which is also independent of CD4+ T‐cell help, but is dependent on CD40 ligation. Furthermore, DC maturation revealed a TAP‐independent mechanism of CD8+ T‐cell priming. Our results also show that class I MHC‐restricted presentation of ovalbumin in ISCOMS by DC is sensitive to chloroquine and brefeldin A but insensitive to lactacystin. We suggest that DC may be the principal antigen‐presenting cells responsible for the priming of CD8+ T cells by ISCOMS in vivo and that targeting these vectors to activated DC may enhance their presentation via a novel pathway of class I antigen processing.
Apolipoprotein E modulates immune activation by acting on the antigen‐presenting cell
Authors: Tenger Charlotta , Zhou Xinghua 
Published: June 2003

SummaryApolipoprotein E (ApoE) is synthesized by a variety of cells including macrophages. These cells activate T lymphocytes by antigen presentation, while the T‐cell cytokine, interferon‐γ, inhibits macrophage ApoE expression. ApoE inhibits T‐cell proliferation in culture but its role in immune responses has been unclear. The ApoE‐deficient (E0) mouse permits an evaluation of the immunological role of ApoE. We have analysed T‐cell responses to an exogenous antigen (ovalbumin) and polyclonal mitogen (concanavalin A) in E0 and ApoE+/+ mice. Macrophages of E0 mice stimulated T‐cell activation more effectively as antigen‐presenting cells than macrophages from ApoE+/+ mice. Both proliferation and interferon‐γ secretion were enhanced in T cells activated in the context of antigen‐presenting cells from E0 mice. Since the macrophage–T‐cell interaction depends on interactions between cell surface molecules, we assessed the expression of such molecules after in vivo stimulation with interferon‐γ. This treatment caused an increased expression of the co‐stimulatory surface proteins CD40 and CD80, and also of the major histocompatibility complex class II molecules I‐Ab on macrophages of E0 mice compared with ApoE+/+. Our data suggest that ApoE inhibits T‐cell activation by reducing the density of immune stimulatory proteins on antigen‐presenting cells.
Efficient antigen presentation of soluble, but not particulate, antigen in the absence of Wiskott–Aldrich syndrome protein
Authors: Westerberg Lisa , Wallin Robert P. A. , Greicius Gediminas , Ljunggren Hans‐Gustaf , Severinson Eva 
Published: June 2003

SummaryB cells and dendritic cells, lacking functional Wiskott–Aldrich syndrome protein (WASP), have aberrant formation of membrane protrusions. We hypothesized that protrusions may play a role in antigen presentation, and consequently, that impaired antigen presentation may be an underlying factor of the immune deficiency in patients with Wiskott–Aldrich syndrome. In this paper, we investigated the antigen presentation capacity of B cells and dendritic cells from WASP knockout mice, using soluble and particulate antigen, to CD4+ T cells from T‐cell receptor transgenic DO11.10 mice. As antigen we used soluble ovalbumin (OVA), a peptide thereof (amino acids 323–339) or bacteria expressing OVA. We found that WASP‐deficient B cells and dendritic cells efficiently processed and presented soluble OVA protein as well as its peptide in vitro, inducing proliferation and cytokine production from CD4+ T cells. Antigen presentation of soluble protein was efficient also in vivo, because immunization of WASP‐deficient mice with OVA elicited proliferation of transferred, fluorescent‐labelled, CD4+ T cells. Although we could detect uptake of bacteria in dendritic cells, processing and presentation of bacterial‐expressed OVA was impaired in WASP‐deficient dendritic cells. In conclusion, our data suggest that WASP is not needed for processing and presentation of soluble antigen, but that efficient presentation of particulate antigen require WASP.
Anti‐human immunodeficiency virus‐gag CD8+ memory T cells generated in vitro from Listeria‐immunized mice
Authors: Rayevskaya Marina , Kushnir Natasha , Frankel Fred R. 
Published: June 2003

SummaryThe goal of vaccination is the generation of immune memory, an immune state that permits rapid and intense recall responses to a pathogen. Considerable effort is being made to understand the nature of memory T cells. We report here that by extending the length of in vitro culture following a single restimulation with specific peptide, preparations of highly enriched, highly active antigen‐specific CD8+ memory T cells could be obtained. These cultures were begun with splenocytes from mice primed by infection either with an attenuated strain of Listeria monocytogenes or vaccinia virus, both expressing the human immunodeficiency virus‐1‐gag gene. In the cultures, antigen‐specific cytotoxic T lymphocyte (CTL) activity reached a maximum at about 9 days and thereafter fell to negligible values. Concomitant with the fall of CTL activity, however, we observed enrichment for a subset of CD11ahigh antigen‐specific gag‐tetramerpos CD8+ T cells. The cells showed little or no 4‐hr CTL activity, but had high delayed (18‐hr) CTL activity, and very high cytolytic activity after restimulation. They rapidly expressed interferon‐γ production. Their growth and survival after sorting was completely dependent on interleukin‐2 or ‐15. As few as 5000 of the fluorescence‐activated cell sorting‐purified cells protected recipients against challenge 3 months after transfer. In response to the challenge, the cells repopulated lymphoid and non‐lymphoid organs and showed a sizeable increase in number. The cells therefore demonstrate high protective activity for long periods of time. These cultured cells are thus a potential source of enriched natural memory T cells for reperfusion studies and in which the mechanisms that underlie the generation, differentiation and persistence of memory can be examined.