bluuebunny/crossref_metadata_2025_split huggingface dataset:
Systemic administration of pituitary adenylate cyclase-activating polypeptide maintains beta-cell mass and retards onset of hyperglycaemia in beta-cell-specific calmodulin-overexpressing transgenic mice
Authors: Tsunekawa Shin , Miura Yoshitaka , Yamamoto Naoki , Itoh Yuji , Ariyoshi Yoh , Senda Takao , Oiso Yutaka , Niki Ichiro 
Published: May 2005

Objective: Pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to play an important role in the regulation of islet function. We investigated its effects in beta-cell-specific calmodulin-overexpressing diabetic (CaMTg) mice, in which we consider that apoptosis of beta cells is the primary defect leading to basal hyperglycaemia.
Methods: CaMTg mice were treated with continuous s.c. infusions of PACAP from 2 to 4 weeks after birth, and were evaluated against littermate non-transgenic (nTg) and saline-treated CaMTg mice as to plasma glucose levels, insulin content, islet function and morphological features.
Results: Remarkable and progressive hyperglycaemia was observed in CaMTg mice, and PACAP treatment blunted this elevation. Insulin secretion from isolated islets demonstrated an impaired response to glucose in CaMTg mice, and PACAP treatment did not cause any improvement. The total pancreatic insulin content in CaMTg mice decreased significantly to 19.1% of that in nTg mice. PACAP treatment of CaMTg mice increased the content to 158% of the value in saline-treated CaMTg mice. The insulin content in isolated islets from CaMTg mice also decreased to 15.9% of that in nTg mice, while PACAP treatment caused a doubling of the value. Immunohistochemical investigation revealed that the insulin-positive islet area was markedly smaller in CaMTg mice and that PACAP treatment significantly expanded the insulin-positive islet area.
Conclusions: These findings indicate that PACAP treatment retards the onset of hyperglycaemia in CaMTg mice by maintaining beta-cell mass and PACAP treatment may potentially be a therapeutic measure for preventing beta-cell exhaustion during hyperglycaemia.
Metformin administration improves endothelial function in women with polycystic ovary syndrome
Authors: Diamanti-Kandarakis E , Alexandraki K , Protogerou A , Piperi C , Papamichael C , Aessopos A , Lekakis J , Mavrikakis M 
Published: May 2005

Objective: The aim of this study was to investigate the endothelial status in young women with polycystic ovary syndrome (PCOS), using a simple and easily reproducible hemodynamic method combined with a biological marker and to evaluate the effect of metformin treatment on these parameters.Design: Descriptive clinical trial.Methods: Forty young women, 20 with PCOS and 20 normal women of similar age and body mass index were studied. Metformin (1700 mg daily) was administered for 6 months to the PCOS group. The endothelium status and the metabolic and hormonal profile were studied in both groups, as well as after metformin, by flow-mediated dilatation (FMD) on the brachial artery and by measurements of plasma endothelin-1 (ET-1) levels.Results: FMD was impaired in the PCOS group when compared with controls (3.24±0.71% vs 8.81±1.07% respectively,P< 0.0001), but this difference normalized after metformin treatment (PCOSpost-metforminvs controls: 8.17±1.26 vs 8.81±1.07%,P= 0.70) since the values significantly improved after metformin treatment (PCOSpre-metforminvs PCOSpost-metformin: 3.24±0.71 vs 8.17±1.26%,P= 0.003). ET-1 levels were significantly higher in the PCOS women compared with the control group (7.23±0.50 vs 4.99±0.69 fmol/l,P= 0.01), they improved significantly after metformin treatment (PCOSpre-metforminvs PCOSpost-metformin: 7.23±0.50 vs 3.57±0.60 fmol/l,P< 0.0001) and their difference compared with the control group was reversed (PCOSpost-metforminvs controls: 3.57±0.60 vs 4.99±0.69 fmol/l,P= 0.13). Metformin administration improved hyperandrogenemia. However, in this study, mathematical methods used to assess insulin resistance failed to show any detected alteration after treatment with metformin.Conclusions: PCOS women were found to exhibit endothelial dysfunction compared with controls, which was reversed 6 months after metformin administration.
Fishing and Natural Mortality of Adult Largemouth Bass in a Tropical Reservoir
Authors: Waters D. Scott , Noble Richard L. , Hightower Joseph E. 
Published: May 2005

AbstractLargemouth bass Micropterus salmoides, an intensively studied sport fish of temperate North America, has been introduced into tropical regions, but with little evaluation of fishing or natural mortality rates. Previous research in Puerto Rico suggested that annual mortality rates are high, but whether the extended spawning season (nearly 6 months annually), high angler harvest, or a combination was the cause of the elevated mortality was unresolved. Using ultrasonic telemetry, we tracked 44 adult largemouth bass over an 18‐month period to quantify patterns of natural, fishing, and total mortality. Using a general capture–recapture model, we estimated the annual instantaneous rates of fishing (0.584, SE = 0.164) and natural mortality (0.310, SE = 0.122). Natural mortality varied seasonally and generally increased during periods of spawning activity; however, fishing mortality was fairly consistent throughout the study. Given the relatively high fishing mortality rate, restrictions on harvest could probably be used to alter the age and size distribution of this population.
A Genetic Assessment of Ohio River Walleyes
Authors: White Matthew M. , Kassler Todd W. , Philipp David P. , Schell Scott A. 
Published: May 2005

AbstractWalleyes Sander vitreus from nine Ohio River pools were examined by means of two independent restriction fragment length polymorphism (RFLP) analyses of mitochondrial DNA, allozyme analysis of nuclear DNA, and microsatellite analysis of nuclear DNA. The primary objective of this project was to document genetic variation and population structuring in walleyes among the nine pools analyzed. Both RFLP analyses revealed the presence of a distinct haplotype that was most abundant in walleyes collected from two tailwaters in the upper Ohio River (river miles 54 and 84), suggesting a remnant native population. The allozyme analysis also revealed differentiation between walleyes with the two haplotypes, even though there were no fixed differences. The microsatellite analysis indicated highly significant structuring among the nine pools analyzed. A lack of microsatellite differentiation between the two haplotypes detected in the same pool suggests that the fish are freely interbreeding. If the unique haplotype is from a remnant native stock of walleyes in the Ohio River, it could serve as a genetic marker to establish a broodstock for stocking walleyes in the upper Ohio River drainage. The second objective of the project was to evaluate the accuracy of field identifications of walleyes, saugers S. canadensis, and their hybrid, saugeyes, and to determine the direction of hybridization. Twenty‐seven percent of the fish identified as walleyes were misidentified (10% were FX hybrids and 17% F1 hybrids). All F1 hybrids were from walleye females and sauger males.
Population Viability Analysis of Atlantic Salmon in Maine, USA
Authors: Legault Christopher M. 
Published: May 2005

AbstractPopulations of Atlantic salmon Salmo salar in eight rivers of Maine, USA, are listed as endangered under the U.S. Endangered Species Act. This listing has required the creation of measurable and objective delisting criteria. One component of these criteria is the determination of the abundance levels associated with recovered populations. Population viability analysis (PVA) was chosen as the method to estimate these recovery levels because it (1) formalizes the combination of information available on the species. (2) quantifies the uncertainty in the population parameters and evaluates the impact of this uncertainty on the probability of extinction, and (3) allows examination of potential management strategies. A PVA specific to the Atlantic salmon populations in Maine was conducted based on the life history characteristics of the endangered populations (i.e., multiple ages of return from sea, kelting, river‐specific habitat limitations, and use of stocking as a recovery tool). The model was verified by using data from a single river and by comparing the results with those of a simpler PVA model. Projections for the eight rivers were conducted for a range of future conditions and management strategies to produce extinction probabilities that managers could use to set recovery criteria. Results beyond extinction risk, such as population age or stage structure, are also shown to be important for management consideration.
Effects of Surgically Implanted Transmitter Weights on Growth and Swimming Stamina of Small Adult Westslope Cutthroat Trout
Authors: Zale Alexander V. , Brooke Carrie , Fraser William C. 
Published: May 2005

AbstractThe generally accepted 2% ratio of transmitter weight to body weight constrains or precludes telemetry studies examining the timing and location of spawning of small adult westslope cutthroat trout Oncorhynchus clarkii lewisi in headwater streams. We empirically determined effects of surgically implanted dummy transmitters ranging in weight from 1 to 5 g on the swimming stamina and growth of small (81.3–206.9 g) adult westslope cutthroat trout in the laboratory to establish acceptable transmitter weights for field studies on this species. Mean growth rates and swimming stamina were not significantly different among treatments, including controls. No precipitous decline or threshold beyond which performance deteriorated markedly was observed. Data collected using telemetered westslope cutthroat trout implanted with transmitters less than about 4% of body weight should therefore approximate information about untelemetered individuals without significant bias. However, we also detected subtle effects on growth within this transmitter weight range related to individual transmitter–body weight ratios (0.5–5.3% initially), and there were indications that swimming stamina was affected similarly. Each 1% increase in transmitter– body weight ratio elicited an 11.6% decrease in growth and a possible 5.6% decrease in swimming stamina at 6 weeks postimplantation. Therefore, transmitter selection should weigh the costs of increased transmitter weight on fish performance against the benefits of longer transmission durations. In the case in which transmitter weights approaching 4% of body weight are necessary to complete a study and slight decreases in performance are not expected to affect findings materially, such weights may be acceptable. In other cases, researchers should choose the lightest possible transmitters that allow study goals to be achieved and not automatically select transmitters weighing 4% of body weight.
The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts
Authors: Isenmann Stefan , Molthagen Martin , Brandner Sebastian , Bartsch Udo , Kühne Guido , Magyar Josef P. , Sure Ulrich , Schachner Melitta , Aguzzi Adriano 
Published: May 2005

AbstractAdhesion molecule on glia (AMOG) represents the β2‐subunit of murine Na, K‐ATPase. Mice carrying a targeted deletion of the AMOG/β2 gene exhibit tremor and limb paralysis at postnatal day (P) 15 and die 2 days after the onset of symptoms. The brains of these mice show edema and swelling of astrocytic end feet However, the cause of death has remained unclear. To identify long‐term consequences of AMOG/β2 deficiency, we have grafted parts of the embryonic telencephalic anlage of AMOG/β2deficient mice into the caudoputamen of wild‐type mice and analyzed the grafts up to 500 days after transplantation. Histological, immunocytochemical, and in situ hybridization techniques were applied to examine histoarchitecture, proliferation, differentiation, and long‐term survival of grafts.AMOG/β2‐deficient telencephalic grafts develop normally and form solid neural tissue that cannot be distinguished from control grafts by morphological features or with immunocytochemical stains for neuronal and glial markers. No signs of degeneration can be found. Expression analysis, however, revealed that no AMOG/β2 protein of possible host origin can be detected in AMOG/β2‐deficient grafts. Graft‐borne astrocytes express neither the AMOG/β1 nor the AMOG/β2 subunit of Na, K‐ATPase as examined with immunocytochemistry and in situ hybridization. These findings indicate that AMOG/β2 is not necessary for loner‐term survival of telenceohalic eraft tissue. © 1995 Wiley‐Liss, Inc.
Early expression of a novel radial glia antigen in the chick embryo
Authors: Prada Francisco A. , Dorado Manuel E. , Quesada Adela , Prada Carmen , Schwarz Uli , de la Rosa Enrique J. 
Published: May 2005

AbstractMonoclonal antibody 3CB2 recognizes an antigen expressed in discrete cell types derived from ectoderm and mesoderm. Biochemical and immunohistochemical studies indicate that the antigen recognized by the antibody is a 55 kDa cytoplasmic protein that may be an intermediate filament associated protein (IFAP). Developmental studies show that 3CB2 antigen is intensely expressed very early in the chick embryo, in the neural tube, myotomes, and in mesenchymal cells of visceral arches and the presumptive facial area. As development proceeds, antigen expression becomes restricted to astrocytes and radial glia cells throughout the brain.A detailed immunohistochemical study of the developing chick retina shows that the expression of 3CB2 antigen at embryonic day 8 (E8) is restricted to Müller cells, with the pattern of expression closely related to their degree of differentiation. We show, by immunocytochemistry labeling of entire Müller cells dissociated from retinas of E16‐E20, that 3CB2 monoclonal is labeling the whole cell. 3CB2 selectively labels Müller cells in the rat and chameleon, but not their retinal horizontal cell axons.3CB2 monoclonal is a very sensitive marker for early differentiating Müller cells. Our results provide evidence that 3CB2 antigen is a cytoskeletal component which may be involved in the morphogenesis of these cells, and also perhaps in the outgrowth of some axons. © 1995 Wiley‐Liss, Inc.
Neural cells from dogfish embryos express the same subtype‐specific antigens as mammalian neural cells in vivo and in vitro
Authors: Gould Robert M. , Fannon Allison M. , Moorman Stephen J. 
Published: May 2005

AbstractNeural cells are classically identified in vivo and in vitro by a combination of morphological and immunocytochemical criteria. Here, we demonstrate that antibodies used to identify mammalian oligodendrocytes, neurons, and astrocytes recognize these cell types in the developing spiny dogfish central nervous system and in cultures prepared from this tissue. Oligodendrocyte‐lineage‐specific antibodies O1, O4, and R‐mAb labeled cells in the 9 cm dogfish brain stem's medial longitudinal fascicle (MLF) and in areas lateral to it. Process‐bearing cells, cultured from the dogfish brain stem, were also labeled with these antibodies. An anti‐lamprey neurofilament antibody (LCM), which recognized 60 and 150 kDa proteins in dogfish brain stem homogenates, labeled axons and neurons in the brain stem and axons in the cerebellum of the dogfish embryo. It also labeled cell bodies and/or processes of some cultured cerebellar cells. An anti‐bovine glial fibrillary acidic protein antibody, which recognized 42–44 kDa protein(s) in dogfish brain stem homogenates, labeled astrocyte‐like processes in the brain stem and cerebellum of the dogfish embryo and numerous large and small flat cells in the cerebellar cultures. These results demonstrate that dogfish oligodendrocytes, neurons, and astrocytes express antigens that are conserved in mammalian neural cells. The ability to culture and identify neural cell types from cartilaginous fish sets the stage for studies to determine if proliferation, migration, and differentiation of these cell types are regulated in a similar fashion to mammalian cells. © 1995 Wiley‐Liss, Inc.
The role of macrophages, perivascular cells, and microglial cells in the pathogenesis of experimental autoimmune encephalomyelitis
Authors: Bauer Jan , Huitinga Inge , Zhao Weiguo , Lassmann Hans , Hickey William F. , Dijkstra Christine D. 
Published: May 2005

AbstractClinical signs of experimental autoimmune encephalomyelitis (EAE) in rats can be suppressed by treatment with liposomes containing dichloromethylene diphosphonate (Cl2MDP liposomes). Here we investigated whether besides the blood‐borne macrophages also ED2+ perivascular cells and microglia are affected by this treatment. For this purpose we examined the central nervous system of bone marrow chimeras in which EAE was induced with encephalitogenic T cells. Quantification of cell numbers of various cell types in inflammatory lesions in the spinal cord showed that after treatment with Cl2MDP liposomes more than 95% of the bone marrow derived (I1‐69+) macrophages were eliminated. In addition the number of ED2+ perivascular cells were seen to be decreased by 68% as compared to ED2+ cells in control liposome treated animals. However the number of these perivascular cells in Cl2MDP liposome treated animals did not differ from the number of perivascular cells in naive animals, indicating that only newly recruited, inflammation associated, ED2+ macrophages were eliminated. Moreover, detection of degenerating nuclei by in situ nick translation (ISNT) in combination with staining for ED1 or ED2 showed that in the perivascular space no degenerating cells were present. Cl2MDP liposome treatment furthermore decreased the numbers of T cells infiltrating the parenchyma by more than 50%. Instead T cells were found in large numbers in the perivascular space. Microglia did not seem to be eliminated by Cl2MDP liposome treatment as shown by the absence of ED1+/ISNT+ cells in the CNS parenchyma. However the number of ED1+(I1‐69−) microglial cells decreased by more than 80%, indicating that the activation of this cell type was impaired. It is concluded that bone marrow derived macrophages play an important role in the pathogenesis of EAE via interactions with lymphocytes and the activation of resident microglia. © 1995 Wiley‐Liss, Inc.
Calcitonin gene‐related peptide and ATP induce immediate early gene expression in cultured rat microglial cells
Authors: Priller Josef , Haas Carola A. , Reddington Martin , Kreutzberg Georg W. 
Published: May 2005

AbstractFactors affecting gene expression in microglial cells were investigated using the induction of immediate early genes in cultured microglia as a model. In particular, the actions of calcitonin gene‐related peptide (CGRP) and ATP, both of which have been proposed as signalling molecules in the activation of glial cells, were evaluated using Northern blotting and in situ hybridization methods. In the presence of CGRP, c‐fos and junB mRNAs accumulated in microglial cultures, whereas no significant change in c‐jun and TIS11 mRNAs occurred. A similar pattern of immediate early gene activation was obtained when adenylate cyclase was stimulated with forskolin. CGRP also stimulated cyclic AMP accumulation with a half‐maximal effect in the range 2–5 nM, suggesting a possible role for cyclic AMP as a mediator of the effects of CGRP on gene expression.In contrast to the selective induction of c‐fos and junB by CGRP and forskolin, ATP led to the accumulation of all four immediate early genes studied, i.e., c‐fos, junB, c‐jun, and TIS11. Similar results were obtained when protein kinase C was stimulated with phorbol ester indicating that the induction of immediate early gene expression by ATP and CGRP involves different intracellular mechanisms. The action of ATP was mimicked by ADP and the poorly hydrolyzable analogues, ADPβS and 2‐methylthio ATP, but not by β,γ‐methylene ATP, AMP, or adenosine, indicating that the receptor mediating the actions of ATP on microglial gene expression is probably of the P2Y‐purinoreceptor type. The results suggest roles for CGRP and ATP as transcriptional activators in microglial cells. © 1995 Wiley‐Liss, Inc.
Ontogeny and cellular expression of MHC and leucocyte antigens in human retina
Authors: Diaz‐Araya Claudia M. , Provis Jan M. , Penfold Philip L. 
Published: May 2005

AbstractWe have investigated the ontogeny of MHC class I, class II, CD45, and macrophage antigens in wholemounts of normal human fetal retina at 10–25 weeks gestation (WG) using monoclonal antibodies and immunogold histochemistry. MHC class I antigens were expressed on retinal vascular endothelial cells and provided a useful marker of vessel organization from 14–25 WG. Microglial cells expressed immunoreactivity to MHC class I, class II, and CD45 antigens from 10 WG (pre‐vascularization) and macrophage S22 (Mac S22) antigen from 14 WG (post‐vascularization), although none of the antigens tested were detected on neuronal or macroglial elements. Microglia expressing MHC, CD45, and macrophage antigens occurred in both ramified and rounded forms with no close correlation being observed between morphology and antigenicity. The numbers of immunoreactive cells labeled with each of the four markers increased steadily throughout gestation in all specimens studied. Equivalent numbers of microglia expressed MHC class I, class II, and CD45 antigens in retinae at similar gestational ages; however, our data indicate that microglia expressing Mac S22 antigen comprise approximately 40% or less of the population of MHC and CD45‐immunoreactive cells during development. Topographical analyses suggest that MHC class I, class II, and CD45‐positive microglia enter the retina from both the peripheral retinal margin and the optic disc from at least 10 WG; Mac S22‐positive cells appear in association with the development of the retinal vasculature and enter the retina via the optic disc after 14 WG. © 1995 Wiley‐Liss, Inc.
Prostaglandin E1, E2, and cholera toxin increase transcription of the brain creatine kinase gene in human U87 glioblastoma cells
Authors: Kuzhikandathil Eldo V. , Molloy George R. 
Published: May 2005

AbstractThe creatine kinase isoenzymes play an important role in maintaining ATP levels in some cell types during times of high energy demand. We have previously shown in primary cell cultures from rat brain that glial cells express much higher levels of brain creatine kinase (CKB) mRNA than neurons. In a separate earlier study we observed that transcription of CKB mRNA in glial cells can be stimulated by a forskolin‐mediated increase in cAMP via a pathway involving protein kinase A (PKA). In this report, we show that the level of CKB mRNA in human U87 glioblastoma cells can be increased by either prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), or cholera toxin (an activator of GαS proteins). The induction of CKB mRNA occurs rapidly (with maximal induction after 6 h), is at the level of transcription, and is mediated specifically through PKA. In addition, the results indicate that both PGE1 and PGE2 use the same or related signal transduction pathways to increase CKB transcription. These results suggest that in glial cells CKB mRNA can be regulated by extracellular signals acting through G‐protein‐coupled receptors. This study may contribute to an understanding of the mechanisms underlying the previously‐reported, early postnatal increase in CKB enzyme activity in rat brain. The results are also discussed with regard to the potential involvement of the expression of prostaglandins and CKB during hypoxia and ischemia. © 1995 Wiley‐Liss, Inc.