bluuebunny/crossref_metadata_2025_split huggingface dataset:
A sequential study of pathological findings in Atlantic halibut, Hippoglossus hippoglossus (L.), throughout one year after an acute outbreak of viral encephalopathy and retinopathy
Authors: Johansen R , Grove S , Svendsen A K , Modahl I , Dannevig B 
Published: May 2004

AbstractFollowing a natural outbreak of viral encephalopathy and retinopathy (VER) at a commercial farm in Norway, surviving Atlantic halibut, Hippoglossus hippoglossus, were sequentially studied for distribution of nodavirus, immune response and histopathology over 1 year. Typical clinical signs and histopathology of VER were observed during the acute stage of the disease. Most of the surviving fish became subclinical carriers of nodavirus with clusters of nodavirus‐containing cells in the central nervous system. Four random samplings of presumably healthy fish were performed from two fish groups, with low and high growth rates respectively, over a 7‐month period. Immunohistochemical (IHC) examination revealed a higher number of nodavirus‐positive cells in fish with a low growth rate than in fish with a high growth rate. All IHC positive fish were also reverse transcriptase polymerase chain reaction (RT‐PCR) positive for nodavirus and for nodavirus antibodies detected by enzyme‐linked immunosorbent assay (ELISA) at all sampling points. The percentage of PCR‐ and ELISA‐positive fish remained high throughout the year, while the number of IHC‐positive fish decreased, especially in the group with a high growth rate. Several other histopathological changes were observed, including pericarditis, steatitis, changes in liver and kidney, and necrosis of the intestinal wall. None of these findings seemed to be related to the nodavirus infection. Nodavirus was reisolated in cell culture from subclinically infected fish one year after the acute VER outbreak, which indicates that the virus was still infectious.
Heart and skeletal muscle inflammation in Atlantic salmon, Salmo salar L.: a new infectious disease
Authors: Kongtorp R T , Kjerstad A , Taksdal T , Guttvik A , Falk K 
Published: May 2004

AbstractHeart and skeletal muscle inflammation (HSMI) is a disease syndrome of unknown aetiology first observed in farmed Atlantic salmon, Salmo salar, in 1999. In the present study we have demonstrated for the first time that HSMI is an infectious disease. It was induced in Atlantic salmon post‐smolts after injection with tissue homogenate from farmed Atlantic salmon previously diagnosed with HSMI. The lesions were also induced in cohabitating salmon given a corresponding injection without tissue homogenate. Six weeks post‐challenge the fish that had been injected with tissue homogenate developed a serious epicarditis and myocarditis with mononuclear cell infiltrations in compact and spongy layers of the heart. Similar lesions were found in cohabitants after 10 weeks. The lesions were consistent with samples from field outbreaks of HSMI. No lesions were found in control fish. A viral aetiology is strongly suggested, as no difference in disease induction between an inoculum containing antibiotics and a non‐treated inoculum was found. Further investigations are required in order to make conclusions regarding the cause and pathogenesis of HSMI.
In vitro interactions between Neoparamoeba sp. and Atlantic salmon epithelial cells
Authors: Butler R , Nowak B F 
Published: May 2004

Abstract Neoparamoeba sp., including the putative aetiological agent of amoebic gill disease in cultured fish (N. pemaquidensis), were incubated in vitro with an Atlantic salmon gill epithelium (RGE‐2) cell line. Proliferation by the amoeba population was dependent upon culture osmolarity; no growth occurred at 330 mm kg−1 but a sixfold increase was observed at 1000 mm kg−1. At 780 mm kg−1 there was a fourfold increase in the amoeba population but a concurrent decrease in RGE‐2 cell density that was significantly greater than that caused by the high culture osmolarity alone. This apparent cytopathic effect (CPE) developed rapidly and resulted in complete cytolysis of the monolayer in 5 days. CPE occurred in multiple foci and presented as cell vacuolation, rounding and clumping, and the rapid clearance of large areas of the cell monolayer. The possibility that CPE is because of the presence of Neoparamoeba sp. derived cytolytic products is discussed in the context of the pathology of the disease in vivo and the occurrence of secreted cytopathogenic compounds in other amoeba species.
Effect of diets containing gossypol on blood parameters and spleen structure in tilapia, Oreochromis sp., reared in a recirculating system
Authors: Garcia‐Abiado M A , Mbahinzireki G , Rinchard J , Lee K J , Dabrowski K 
Published: May 2004

AbstractThe high cost of fish meal in tilapia diets warrants the potential use of cottonseed meal (CSM) as an alternative source of high quality protein. The effects of varying levels of CSM (0, 25, 50, 75 and 100%) as fish meal protein replacement on growth, blood parameters, spleen characteristics, free and bound gossypol in blood plasma, haemoglobin and haematocrit were determined in tilapia. Gossypol (C30H30O8) is a polyphenolic substance found in cottonseed that has known toxic effects in fish. Tilapias (n = 219, average weight = 11.3 ± 3.9 g) were randomly distributed into 15, 32‐L glass aquaria, representing five dietary treatments and three replicates per treatment. Each aquarium containing 13–16 fish was supplied with thermoregulated, recirculating water (27 ± 1 °C) at 1 L min−1 flow rate and photoperiod was constant (12 h L/12 h D). Fish fed 25–50% CSM protein replacement showed similar body weights and total lengths as the controls at the completion of the 16‐week trial. Fish fed 75 and 100% CSM protein replacement showed a significant decline in body weight and total length. Fish fed 25–100% CSM protein replacement had significantly lower haematocrit and haemoglobin (ANOVA/LSD, P < 0.05) compared with levels in controls. The decline was most prominent in groups fed diets with 50–100% CSM protein replacement. Total and free gossypol concentrations of blood plasma significantly increased with increasing levels of CSM replacement (P < 0.05). No gossypol was found in blood plasma of fish from the control group. The occurrence of immature and abnormal erythrocytes was significantly greater among fish fed 75 and 100% CSM diets compared with fish fed 0–50% CSM diets. Spleen‐somatic index (spleen weight/body weight × 100) did not differ between control fish and fish fed 50–100% CSM diets. Spleen abnormalities, such as large depositions of haemosiderin and melanin pigments and proliferation of melano‐macrophage centres, lymphocytic depletion of the white pulp areas (hypocellularity), and presence of vacuoles and necrotic areas were observed among fish fed 50–100% CSM protein diets. In general, the pathological effects of gossypol in tilapia (low haemoglobin and haematocrit levels, abundance of immature red blood cells or polychromatocytes, abnormal spleen morphology) were similar to the effects of vitamin E and/or vitamin C deficiencies observed in other studies.
Oestrogenic Regulation Of Brain Angiotensinogen
Authors: Greenland K. J. , Sernia C. 
Published: May 2004

AbstractOestrogens are now recognized as playing a regulatory role on components of the systemic renin–angiotensin system, such as its precursor, angiotensinogen (AGT). In the brain, this role is poorly understood. The aim of this study was to investigate the influence of oestrogens on brain AGT of female rats at different stages of the oestrous cycle, in pregnancy and following ovariectomy with and without hormone replacement. AGT content of different brain regions was also studied in male rats treated with oestrogens. The brain was divided into five regions: cortex, cerebellum, brainstem, midbrain and thalamus/hypothalamus, and AGT was measured by direct radioimmunoassay using a highly specific AGT antibody. Cyclical fluctuations in AGT content were observed in all regions except the cerebellum over the course of the 4‐day oestrous cycle, with peak concentrations at estrus and lowest concentrations at metestrus. Following ovariectomy, brain AGT was significantly decreased in the thalamic/hypothalamic region, an effect that was reversed by oestrogen‐replacement. In pregnant rats, AGT contents were elevated in the brainstem region. Oestrogen treatment of male rats induced significant increases in AGT concentrations in all areas except the cortex. In summary, these results show that oestradiol has actions on brain AGT that are region‐specific and dependent on the particular physiological and reproductive context. Moreover, the changes in AGT concentrations in the oestrous cycle suggest the involvement of other factors besides oestrogen. Finally, this study supports the view that the brain renin–angiotensin system has a broad role in oestrogen‐modulated brain functions beyond those specific to the hypothalamic–pituitary–ovarian axis.
Gonadectomy Reverses The Sexually Diergic Patterns Of Circadian and Stress‐Induced Hypothalamic‐Pituitary‐Adrenal Axis Activity In Male and Female Rats
Authors: Seale J. V. , Wood S. A. , Atkinson H. C. , Bate E. , Lightman S. L. , Ingram C. D. , Jessop D. S. , Harbuz M. S. 
Published: May 2004

AbstractEnhanced corticosterone release by female compared to male rats under basal and stress conditions is well documented. The demonstration that gonadectomy enhances stress‐induced corticosterone secretion in male rats, but reduces such levels in female rats, suggests a causal association between gonadal steroids and corticosterone release. The present study examined the corticosterone profile of sham gonadectomized and gonadectomized female and male rats under basal and stress conditions. An automated sampling system collected blood from each freely moving, unanaesthetized rat every 10 min (i) over a 24‐h period; (ii) following noise stress; and (iii) following an immune‐mediated stress (lipopolysaccharide, LPS). Plasma was analysed for corticosterone content using radioimmunoassay. Castration resulted in a significant increase in basal corticosterone release compared to the sham‐castrated male rats. Pulsar analysis revealed a significant two‐fold increase in the number of corticosterone pulses over 24 h. Corticosterone increases in response to noise stress and to LPS injection were enhanced following castration. Conversely, ovariectomy resulted in a two‐fold reduction in the number of corticosterone pulses as well as the stress response compared to sham‐ovariectomized female rats. Arginine vasopressin (AVP), corticotrophin‐releasing hormone (CRH) and glucocorticoid receptor mRNAs in the paraventricular nucleus and pro‐opiomelanocortin (POMC) mRNA in the anterior pituitary were analysed post‐LPS administration by in situ hybridization. Significantly higher values were found for AVP, CRH and POMC mRNAs examined for sham females and castrated males compared to sham males and ovariectomized females. This study confirms previous reports concerning the influence of gonadal factors in regulating HPA axis activity and stress responsiveness. The present results extend these observations to the regulation of the dynamic pattern of corticosterone release under basal conditions and suggests that this alteration in pulsatility is important for the differences in stress responsiveness when comparing males and females.
Appetite Regulatory Neuropeptides are Expressed in the Sheep Hypothalamus Before Birth
Authors: Mühlhäusler B. S. , McMillen I. C. , Rouzaud G. , Findlay P. A. , Marrocco E. M. , Rhind S. M. , Adam C. L. 
Published: May 2004

AbstractIn the adult, a hypothalamic neural network acts to maintain energy balance in response to nutritional feedback from the periphery. Although there is an immediate requirement for this system to be functional at birth, it is unknown whether the components of this central neural network are expressed in the developing brain before birth. We therefore examined in the fetal sheep hypothalamus during late gestation gene expression for leptin receptor (OB‐Rb) and neuropeptides that regulate energy balance in the adult. Brains were collected from fetal sheep at 110 days (n = 12) and 140 days of gestation (n = 5) (term = 150 days) and gene expression was detected in all hypothalami using in situ hybridization with radiolabelled riboprobes for OB‐Rb, neuropeptide Y (NPY), agouti‐related peptide, pro‐opiomelanocortin and cocaine‐ and amphetamine‐regulated transcript (CART). All mRNAs were expressed in the arcuate nucleus of fetuses at both time points. Additional sites of mRNA expression were the dorsomedial hypothalamus (DMH) for NPY, the paraventricular nucleus (PVN), ventromedial hypothalamus (VMH) and lateral hypothalamic area for CART, and the DMH, PVN and VMH for OB‐Rb. We have therefore demonstrated that adult‐like localization of gene expression for OB‐Rb and key appetite regulatory neuropeptides is established in the ovine hypothalamus before birth. Thus, the fetus possesses a central appetite regulatory neural network with the potential to respond to changes in nutrient supply, which could impact on energy balance regulation both before and after birth.
Immunocytochemical Investigation of Nuclear Progestin Receptor Expression within Dopaminergic Neurones of the Female Rat Brain
Authors: Lonstein J. S. , Blaustein J. D. 
Published: May 2004

AbstractProgesterone influences most processes involved in female reproduction, including ovulation, sexual behaviour, pregnancy, parturition, lactation and maternal behaviour. One neurotransmitter through which progesterone might regulate many of these functions is dopamine. To determine where in the brain progesterone might alter dopaminergic activity necessary for these and other processes in rats via cell nuclear progestin receptors, ovariectomized rats were injected subcutaneously with either 4 µg oestradiol benzoate to induce high levels of hypothalamic progestin receptor expression, or oil, and perfused 48 h later. Dual‐label immunocytochemistry was used to visualize cells having immunoreactivity (ir) for progestin receptors and tyrosine hydroxylase, a rate‐limiting enzyme for dopamine synthesis. Many cells containing both progestin receptor‐ir and tyrosine hydroxylase‐ir were found throughout the periventricular hypothalamus of oestradiol‐treated females. Conversely, very few cells in the hypothalamus of oil‐treated controls contained progestin receptor‐ir and, consequently, few dual‐labelled cells were found in this group. The greatest percentage of tyrosine hydroxylase immunoreactive cells expressing progestin receptors in oestradiol‐treated females was in, or near, the arcuate nucleus (A12 group), where up to 55% of tyrosine hydroxylase‐expressing cells coexpressed progestin receptors. Notably, dual‐labelled cells in oestradiol‐treated females were also found more rostrally than previously reported, with approximately 15–20% of tyrosine hydroxylase‐ir cells in the preoptic area/anterior hypothalamus (A14 group) also containing progestin receptor‐ir. No dual‐labelled cells were found for either group in the posterodorsal hypothalamus (A11 group), zona incerta (A13 group), retrorubral field (A8 group), ventral tegmental area (A10 group) or substantia nigra (A9 group) because little or no progestin receptor‐ir was found in these sites. These data provide new information about the neural substrate where progesterone might regulate dopamine release in the preoptic area/anterior hypothalamus. Using more sensitive techniques than those used previously, they also confirm the relationship between progestin receptor and tyrosine hydroxylase in the arcuate nucleus, which could be important for the regulation of prolactin release throughout the female reproductive cycle. Additionally, although progesterone alters mesolimbic and nigrostriatal dopamine release, and the numerous behaviours that these pathways influence, these data again suggest that it does not do so via nuclear progestin receptor in dopaminergic cells of the ventral tegmental area and substantia nigra.
Cellular Expression of V1a Vasopressin Receptor mRNA in the Female Rat Preoptic Area: Effects of Oestrogen
Authors: Kalamatianos T. , Kalló I. , Goubillon M‐L. , Coen C. W. 
Published: May 2004

AbstractThe preovulatory luteinizing hormone (LH) surge in female rats is dependent upon signals from the suprachiasmatic nucleus (SCN), the site of a dominant circadian pacemaker. Various lines of evidence indicate that arginine‐vasopressin (AVP)‐containing projections from the SCN to the preoptic area (POA) contribute to the production of the surge of LH‐releasing hormone (LHRH). These actions may be mediated by V1a because the transcript for this AVP receptor subtype is predominant within the POA of the female rat. In this study, in situ hybridization histochemistry was used to examine V1a mRNA expression, either by itself or together with LHRH or glutamic acid decarboxylase 65 (GAD65) mRNA, within the POA of ovariectomized rats in the presence or absence of oestrogen. V1a mRNA was found in cells across the rostro‐caudal axis of the POA; some were in close proximity to cells expressing LHRH mRNA. Coexpression of V1a and LHRH mRNAs was detected only very rarely. By contrast, cells with V1a mRNA commonly displayed GAD65 mRNA. The density of V1a mRNA‐expressing cells was particularly high within the anteroventral periventricular nucleus; at this site, V1a mRNA expression was elevated following oestrogen treatment. The present results indicate that V1a‐mediated AVP actions may influence LHRH release via cells in the immediate vicinity of LHRH neurones and/or via oestrogen‐regulated cells in the anteroventral periventricular nucleus, which is a site that lacks LHRH neurones but plays an essential role in initiating the preovulatory LH surge.
Chronic Glucocorticoid Deficiency‐Induced Abnormal Aggression, Autonomic Hypoarousal, and Social Deficit in Rats
Authors: Haller J. , Halász J. , Mikics É. , Kruk M. R. 
Published: May 2004

AbstractCertain aggression‐related psychopathologies are associated with decreased glucocorticoid production and autonomic functions in humans. We have previously shown that experimentally‐induced chronic glucocorticoid deficiency leads to abnormal forms of attack in rats. Here, we compared the effects of acute and chronic glucocorticoid deficiency on aggressive behaviour, autonomic responses to challenges, and anxiety. Glucocorticoid synthesis was blocked acutely by the glucocorticoid synthesis blocker metyrapone or chronically by adrenalectomy and low glucocorticoid replacement (ADXr). As shown previously, chronic glucocorticoid deficiency facilitated aberrant attacks directed towards the most vulnerable parts of the opponent's body. The acute inhibition of glucocorticoid synthesis lowered aggressive behaviour without affecting attack targeting. In a different experiment, ADXr rats and their sham‐operated controls were exposed to different challenges whereas their heart rate and locomotion were telemetrically recorded. Autonomic responses to social challenges were lowered by chronic, but not by acute glucocorticoid deficiency. Autonomic responses to the elevated plus‐maze were only slightly affected by chronic glucocorticoid deficiency. Locomotor behaviour was not affected in either challenge; thus, the altered autonomic reactions were not due to interference from workload. The behaviour of ADXr rats was similar to that of sham‐operated controls in the elevated plus‐maze, but ADXr rats showed reduced social interactions in the social interaction test. Our data demonstrate that, in rats, chronic but not acute glucocorticoid deficiency induces abnormal attack patterns, deviant cardiovascular responses and social deficits that are similar to those seen in abnormally violent humans. Thus, the similar correlations found in humans probably cover a causal relationship. Experimentally‐induced glucocorticoid deficiency may be used to assess the mechanisms underlying glucocorticoid deficiency‐induced abnormal forms of aggressiveness.
Stimulation of Luteinizing Hormone Subunit Gene Expression by Pulsatile Intracerebroventricular Microinjection of Galanin in Female Rats
Authors: Gajewska A. , Zwierzchowski L. , Kochman K. 
Published: May 2004

AbstractAlthough galanin, which exerts its effects both at the hypothalamic and pituitary level, has been implicated as an important neuroendocrine regulator of hypothalamic‐pituitary‐gonadal axis activity, there is a lack of data concerning its involvement in the regulation of gonadotropin subunit gene expression. To elucidate whether galanin can influence luteinizing hormone (LH) subunit mRNA content, as well as affect gonadotropin‐releasing hormone (GnRH) receptor activity, a model based on pulsatile (one pulse per hour over 5 h) galanin (1 nM) microinjections directly into the third cerebral ventricle of ovariectomized (OVX) and/or oestrogen/progesterone‐pretreated rats was used. Furthermore, to determine galanin effects on GnRH‐induced LH subunit mRNA synthesis, a cocktail of 1 nM GnRH and 1 nM galanin was coadministered in a pulsatile manner to OVX/steroid primed rats. Subsequently, to obtain data concerning the role of galanin receptors in the regulation of pituitary α (common to LH, follicle‐stimulating hormone, thyroid‐stimulating hormone) and LHβ subunit gene expression, OVX/oestrogen/progesterone rats received microinjections of 1 nM of the receptor antagonist galantide and 1 nM of galanin. In this case, both substances were administered separately, with a 30 min lag, according to which each galantide pulse always preceded a galanin pulse. Northern‐blot analysis revealed that intracerebroventricular pulsatile galanin injections were effective in stimulation of both α and LHβ subunit mRNA levels and that this effect was apparently steroid‐dependent. Moreover, galanin also up‐regulated GnRH receptor functional parameters (affinity and maximum binding capacity) but was ineffective in potentiating GnRH‐induced accumulation of both subunit mRNAs. The results from the study also indicate that galanin acts through its own receptor(s) because a receptor antagonist, galantide, significantly reduced the stimulatory effect exerted by galanin on the expression of both LH subunit genes in vivo.
Endolysosomal Processing of Exogenous Antigen into Major Histocompatibility Complex Class I‐Binding Peptides
Authors: Chen L. , Jondal M. 
Published: June 2004

AbstractAn alternative endolysosomal pathway has recently been suggested for the processing of MHC‐I‐binding peptides, and peptide/MHC‐I complexes have been demonstrated in this compartment. However, it remains unclear where in the antigen‐presenting cells such peptides are processed, in the endolysosomes themselves or in the proteasomal complex. Here, we have investigated this using monoclonal antibodies specific for the immunodominant SIINFEKL/Kb complex (25‐D1) or for the carbohydrate part of Db‐ or Kb‐binding glycopeptides in combination with inhibitors for classical and endolysosomal MHC‐I‐processing pathways. Alternative processing was detected in both wt and TAP1–/– immature DC (iDC) as the expression of SIINFEKL/Kb complexes on the surface of OVA‐treated cells in the presence of Brefeldin A (BFA) or lactacystin and their absence in the presence of the lysosomotropic amines ammonium chloride, chloroquine and methylamine. Internalized Db‐ and Kb‐binding glycopeptides, detected with high specificity using an anti‐galabiose (Gal2) monoclonal antibody, were found to appear on the cell surface of BFA‐treated cells after intracellular MHC‐I‐binding. Peptide exchange in Kb was demonstrated as the gradual appearance of SIINFEKL/Kb complexes on BFA‐treated cells which earlier had been saturated with another Kb‐binding peptide. Our data support the presence of a fully functional endolysosomal processing pathway in iDC guided by the chaperone function of MHC‐I molecules.