bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dietary effect of different high‐fat diet on rat liver stereology
Authors: Aguila Márcia Barbosa , Pinheiro Alessandra da Rocha , Parente Lyana Barbosa , Mandarim‐de‐Lacerda Carlos Alberto 
Published: September 2003

Abstract:Background/aims: Dietary habits are considered to be responsible for a fatty liver. The aims of this work are to study the effects of different lipid sources on rat hepatic structure.Methods: Twenty 21‐day‐old to 18‐month‐old male rats were fed one of the following diets: soybean oil, canola oil, lard and egg yolk (LE), or canola oil+lard and egg yolk (CA+LE). The blood serum triglyceride samples were analyzed. The following hepatic biometry and the stereology parameters were determined: densities of volume (Vv) and surface (Sv), absolute volume (V) and surface (S) of the hepatocytes (h), fat globules (g), and hepatic sinusoids (s), and numerical density of the hepatocytes (Nv[h]).Results: The largest values of Vv[h], Sv[h], V[h], and S[h] were found in the LE group. However, the largest values of Vv[g], Sv[g], and S[g] were found in the CA+LE group, and the smallest values of those parameters were found in the LE group. On the other hand, V[g] was larger in the CA+LE group. Vv[s] and V[s] were larger in the LE group and smaller in the CA+LE group.Conclusion: Long‐term administration of canola oil or soybean oil resulted in similar effects on hepatocytes, hepatic sinusoids, and fat globules. Long‐term administration of lard and egg yolk attenuates hepatic fat accumulation and increases hepatic sinusoids. The administration of the canola oil and lard and egg yolk mixture increases hepatic fat accumulation, reducing the hepatic sinusoids.
Inhibition of nuclear factor κB and phosphatidylinositol 3‐kinase/Akt is essential for massive hepatocyte apoptosis induced by tumor necrosis factor α in mice
Authors: Imose Motoaki , Nagaki Masahito , Naiki Takafumi , Osawa Yosuke , Brenner David A. , Asano Takahiko , Hayashi Hideki , Kato Tomohiro , Moriwaki Hisataka 
Published: September 2003

Abstract:Background/aims: Tumor necrosis factor (TNF)‐α itself does not induce liver injury in normal mice or hepatocytes. Rather, this event, especially in vitro, is explained by the fact that the TNF‐α/TNF receptor system not only triggers downstream signals leading to apoptosis but also induces an antiapoptotic pathway through the activation of nuclear factor (NF)‐κB. The aim of this study was to determine whether inhibition of antiapoptotic pathways influences the susceptibility of mice to TNF‐α. Here, we focused on the roles of NF‐κB and phosphatidylinositol 3‐kinase (PI3K)‐regulated serine/threonine kinase Akt.Methods: TNF‐α was administered to BALB/c mice after treatment with an adenovirus expressing a mutant form IκBα (Ad5IκB), the PI3K inhibitor wortmannin, or both. Liver injury was assessed biochemically and histologically. The expression of Bcl‐2 family members and caspase activity were examined.Results: In the mice livers, treatment with Ad5IκB or the wortmannin suppressed the activation of NF‐κB or Akt, respectively. Suppression of either NF‐κB or Akt showed a slight increase in transaminase levels and focal liver cell death after TNF‐α administration. However, in mice treated with both Ad5IκB and wortmannin, TNF‐α administration resulted in massive hepatocyte apoptosis and hemorrhagic liver destruction in mice. The combination of Ad5IκB, wortmannin, and TNF‐α markedly increased the activation of caspase‐3 and ‐9, and activated caspase‐8 to a lesser degree, suggesting that TNF‐α‐induced hepatocyte apoptosis is dependent on type II cell death signaling pathway, probably through the mitochondria. Inhibition of the NF‐κB and PI3K/Akt pathways had no effect on expression of Bcl‐2 families.Conclusion: The inducible activation of NF‐κB and constitutive activation of Akt regulate hepatocyte survival against TNF‐α, which occurs independent of Bcl‐2 families.
The production, storage and viability of seeds of Acacia karroo and A. nilotica in a grassy savanna in KwaZulu‐Natal, South Africa
Authors: Walters Michele , Milton Suzanne J. 
Published: September 2003

AbstractAfrican Acacias are often major contributors to the progressive increase in the woody component of savannas, a phenomenon commonly referred to as bush encroachment. They produce large quantities of seed and may have large soil‐stored seed banks. In Hluhluwe–Umfolozi Park, the number of adult Acacia nilotica trees per hectare far exceed that of A. karroo adults. The relative dominance is reversed in the juvenile stage with A. karroo outnumbering A. nilotica threefold outside closed woodlands. Acacia karroo trees were smaller than A. nilotica trees on average, but produced more seeds for a given basal diameter size class. Acacia karroo showed less bruchid infestation than A. nilotica at all stages of pod development. Unlike A. nilotica, a proportion of A. karroo seeds was able to germinate after bruchid attack. We detected no difference between the two species in the soil‐stored seed bank or in the viability of seeds found in the seed bank.
Age‐related changes in defensive traits of Acacia tortilis Hayne
Authors: Gowda Juan H. , Palo R. Thomas 
Published: September 2003

AbstractThe theory of plant defences proposes that investments in physical and chemical defences are driven by the risk of herbivore damage, and limited by the cost of producing the particular defensive trait in terms of resources that could be directed to other sinks, such as growth and reproduction. We sampled twigs of 18 mature Acacia tortilis trees and their cohort of juveniles to test some predictions of this hypothesis.We expected a higher allocation of defensive traits to leaves and twigs in the young plants than in the mature ones as a result of a higher risk of damage by ungulates at the juvenile stage. Our results show that the juvenile plants produce more spines along their twigs, but have lower concentrations of phenolic compounds in their leaves than in the mature ones.We also expected a negative relation between the concentration of foliar nutrients and phenolic compounds, as predicted by the carbon/nutrient hypothesis. Only mature plants showed this pattern.Reproduction (in mature plants) and water stress (in juvenile plants) did not relate to allocation to secondary compounds as predicted by current hypotheses of plant defence.
The diet of a small group of extralimital giraffe
Authors: Parker D. M. , Bernard R. T. F. , Colvin S. A. 
Published: September 2003

AbstractGiraffe are extralimital in the Eastern Cape Province, South Africa where recent local introductions have persisted despite limited research into their impact on the indigenous flora. The diet of 15 giraffe at the Shamwari Game Reserve was recorded by direct observation during summer (March/April) and winter (July/August) 2001, quantifying diet by frequency of occurrence (individual records scored and expressed as a percentage of the total). Preference indices were also calculated. Habitat use was measured by the number of hours giraffe fed in different habitats. The diet comprised of 14 plant species, the most important species being Rhus longispina (47.9%), Acacia karroo (25.7%) and Euclea undulata (17.6%). Importance of R. longispina, A. karroo and Tarchonanthus camphoratus fluctuated seasonally. Rhus longispina was more important in winter with a corresponding decrease in feeding on A. karroo. Tarchonanthus camphoratus was only consumed during summer. Acacia karroo thickets (previously disturbed areas) were utilized most (summer 12 h; winter 9 h), with alternative habitats utilized more often in winter than in summer. We suggest that the seasonal fluctuation in the importance of R. longispina & A. karroo reflects the deciduous nature of A. karroo.
Determination of the selenium requirement in kittens*
Authors: Wedekind K. J. , Howard K. A. , Backus R. C. , Yu S. , Morris J. G. , Rogers Q. R. 
Published: September 2003

SummaryThe purpose of this study was to determine the selenium (Se) requirement in kittens. Thirty‐six specific‐pathogen‐free kittens (9.8 weeks old) were utilized in a randomized complete block design to determine the Se requirement in cats with gender and weight used as blocking criteria. Kittens were fed a low Se (0.02 mg/kg Se) torula yeast‐based diet for 5 weeks (pre‐test) after which an amino acid‐based diet (0.027 mg Se/kg diet) was fed for 8 weeks (experimental period). Six levels of Se (0, 0.05, 0.075, 0.10, 0.20 and 0.30 mg Se/kg diet) as Na2SeO3 were added to the diet and were used to construct a response curve. Response variables included Se concentrations and Se‐dependent glutathione peroxidase activities (GSHpx) in plasma and red blood cells (RBC) as well as plasma total T3 (TT3) and total T4 (TT4). No significant changes in food intake, weight gain or clinical signs of Se deficiency were noted. Estimates of the kitten's Se requirement (i.e. breakpoints) were determined for RBC and plasma GSHpx (0.12 and 0.15 mg Se/kg diet, respectively), but no definitive breakpoint was determined for plasma Se. Plasma TT3 increased linearly, whereas plasma TT4 and the ratio of TT4 : TT3 decreased in a quadratic fashion to dietary Se concentration. The requirement estimate determined in this study (0.15 mg Se/kg) for kittens is in close agreement with other species. As pet foods for cats contain a high proportion of animal protein with a Se bioavailability of 30%, it is recommended that commercial diets for cats contain 0.5 mg Se/kg DM.
Molecular Epidemiology of Classical Swine Fever in the Russian Federation
Authors: Vlasova A. , Grebennikova T. , Zaberezhny A. , Greiser‐Wilke I. , Floegel‐Niesmann G. , Kurinnov V. , Aliper T. , Nepoklonov E. 
Published: September 2003

SummaryThe ability to discriminate between various classical swine fever virus (CSFV) strains and isolates is a prerequisite for following the spread of the virus after an outbreak. To determine the relatedness between Russian CSFV isolates from different geographical regions, three fragments of the viral genome (5′ NTR, the variable region of the E2 gene and a fragment of the NS5B gene) were sequenced and used for genetic typing. Thirty‐one field isolates were obtained from CSF outbreaks which occurred between 1994 and 1999. In addition, three attenuated strains were included in the study, namely the LK and CS vaccine strains, and the moderately virulent 238H isolate. The vaccine strains have been used in Russia for more than 30 years. Our results showed that all field isolates are in subgroup 1.1 together with Alfort 187 and with the highly virulent strain Shimen. In contrast, the CS and LK vaccine strains belong to subgroup 1.2. While there is no evidence for the reversion of the two vaccine strains to wild type, it is feasible that the highly virulent Shimen strain, which has been used as a challenge strain for many years, contributed to field strain generation. The Russian field isolates from the 1990s can be distinguished from the CSF virus isolates which occurred in the EU Member States in the same decade, as here all outbreaks were caused by CSF viruses belonging to subgroup 2.
Psittacine Beak and Feather Disease: a First Survey of the Distribution of Beak and Feather Disease Virus Inside the Population of Captive Psittacine Birds in Germany
Authors: Rahaus Markus , Wolff Manfred H. 
Published: September 2003

SummaryPsittacine beak and feather disease (PBFD) is the most common viral disease of wild and captive psittacine birds. Here, we designed the first survey to investigate the existence of subclinical infections and the distribution of the causative agent named beak and feather disease virus (BFDV) inside the population of captive psittacine birds in Germany. DNA was isolated from feathers of 146 symptom‐free birds from 19 different genera (all psittaformes) taken from 32 independent breeders from all over Germany. The presence of BFDV was analysed by performing polymerase chain reaction assays. Fifty‐eight (39.2%) samples were found to be positive for BFDV. As expected, there was no significant predominance of one sex to be infected with BFDV.
Long‐term effects of a single exposure to immobilization stress on the hypothalamic–pituitary–adrenal axis: transcriptional evidence for a progressive desensitization process
Authors: Vallès Astrid , Martí Octavi , Armario Antonio 
Published: September 2003

AbstractIn the present work we have characterized the long‐term influence of a single exposure to the stress of immobilization (IMO) on the hypothalamic–pituitary–adrenal (HPA) axis of adult rats. Rats without prior stress (control) and rats exposed to IMO for 2 h on day 1 (IMO+4wk) or on day 21 (IMO+1wk) were killed on day 28, either without stress (basal), immediately after IMO for 1 h (IMO), or 1 h after termination of IMO (post‐IMO). IMO caused a strong activation of c‐fos mRNA and corticotropin‐releasing factor (CRF) and vasopressin (AVP) heteronuclear RNA (hnRNA) in the paraventricular nucleus of the hypothalamus in control rats; this activation was essentially maintained in the post‐IMO period. The overall AVP hnRNA response to day 28 stress was not affected by prior stress. Post‐IMO c‐fos mRNA and CRF hnRNA levels were lower in previously stressed rats, as compared with controls. Whereas the effect of prior IMO on both peripheral HPA hormones and c‐fos mRNA was maximal in IMO+1wk rats, the effect of prior stress on CRF hnRNA was only observed in IMO+4wk rats. The present data indicate that prior single IMO triggers a process of desensitization of the HPA responsiveness to IMO over the course of the following weeks. Although the various components of the HPA axis were modified in the same direction, a clear temporal dissociation was found among them, revealing the fine tuning of stress‐induced activation of the HPA axis.
Localization of the GABAergic and non‐GABAergic neurons projecting to the sublaterodorsal nucleus and potentially gating paradoxical sleep onset
Authors: Boissard Romuald , Fort Patrice , Gervasoni Damien , Barbagli Bruno , Luppi Pierre‐Hervé 
Published: September 2003

AbstractWe recently determined in rats that iontophoretic application of bicuculline or gabazine [two GABAa antagonists] and kainic acid (a glutamate agonist) in the sublaterodorsal nucleus (SLD) induces with a very short latency a paradoxical sleep‐like state. From these results, we proposed that GABAergic and glutamatergic inputs to the SLD paradoxical sleep (PS)‐executive neurons gate the onset of PS [R. Boissard et al. (2002) Eur. J. Neurosci., 16, 1959–1973]. We therefore decided to determine the origin of the GABAergic and non‐GABAergic inputs to the SLD combining ejection of a retrograde tracer [cholera‐toxin B subunit (CTb)] with glutamate decarboxylase (GAD) immunohistochemistry. The presence of GAD‐immunoreactive neurons in the SLD was confirmed. Then, following CTb ejections centred on the SLD, combined with GAD and CTb immunohistochemistry, double‐labelled cells were observed in the mesencephalic and pontine reticular nuclei and to a lesser extent the parvicellular reticular nucleus. A large number of GAD‐negative retrogradely labelled cells was also seen in these structures as well as in the primary motor area of the frontal cortex, the central nucleus of the amygdala, the ventral and lateral bed nucleus of the stria terminalis, the lateral hypothalamic area, the lateral and ventrolateral periaqueductal grey and the lateral paragigantocellular reticular nucleus. From these results, we propose that the activation of PS‐executive neurons from the SLD is due to the removal of a tonic inhibition from GABAergic neurons localized in the SLD, and the mesencephalic and pontine reticular nuclei. Strong non‐GABAergic inputs to the SLD could be excitatory and responsible for the tonic glutamatergic input on the PS‐on neurons we have previously described. They could also terminate on SLD GABAergic interneurons and be indirectly responsible for the inhibition of the PS‐on neurons during waking and slow‐wave sleep.
Non‐steroidal anti‐inflammatory drugs mediate increased in vitro glial expression of apolipoprotein E protein
Authors: Aleong Rosanne , Aumont Nicole , Dea Doris , Poirier Judes 
Published: September 2003

AbstractEpidemiological studies have shown that use of non‐steroidal anti‐inflammatory drugs (NSAIDs) by the elderly is associated with a decreased relative risk and a delayed onset of Alzheimer's disease (AD). In contrast, the apolipoprotein E (apoE) gene has proven to be a risk factor for AD with apoE ε4 AD patients having been found to show lower levels of brain apoE. In the present study, treatment of primary rat mixed glial cell cultures with the common NSAIDs, indomethacin and aspirin, induced significant increases in extracellular apoE protein levels. Similarly, treatment of primary rat astrocyte cell cultures with aspirin and a cyclooxygenase (COX)‐2‐selective aspirin derivative also stimulated significant increases in apoE protein. However, astrocyte and mixed glial apoE protein levels were significantly reduced following exposure to COX‐2‐specific indomethacin amides and an inactive indomethacin derivative. ApoE protein modulation was observed at physiological and subphysiological concentrations well below the COX inhibition IC50 values of the NSAIDs used, suggestive of a COX‐independent mechanism. In contrast to these results, indomethacin and aspirin treatment failed to induce any significant changes in apoE mRNA levels. The failure of NSAIDs to significantly alter apoE expression may have been indicative of a nontranscriptional mechanism of apoE protein induction. Consequently, NSAID‐induced increases in apoE protein may enhance apoE‐mediated immunosuppression and compensatory synaptic plasticity, potentially resulting in decreased AD risk and delay of disease onset.
Exogenous erythropoietin protects against dorsal root ganglion apoptosis and pain following peripheral nerve injury
Authors: Campana W. Marie , Myers Robert R. 
Published: September 2003

AbstractErythropoietin (Epo) has been shown to have potent anti‐apoptotic activity in central nervous system neurons in animal models of ischaemic injury. Recently, Epo and its receptor (EpoR) have been identified in the peripheral nervous system [Campana & Myers (2001), FASEB J., 15, 1804–1806]. Herein, we demonstrate that in painful neuropathy caused by L5 spinal nerve crush (SNC), therapy with recombinant human Epo (rhEpo) reduced dorsal root ganglion (DRG) apoptosis and pain behaviours. Quantification of both DRG neurons and satellite cells revealed that vehicle‐treated, crush‐injured DRGs had 35.5 ± 8.3% apoptotic neurons and 23.5 ± 2.36% satellite cells compared with 7.5 ± 6.3% apoptotic neurons and 6.4 ± 3.94% satellite cells in rhEpo‐treated, crush‐injured DRGs (P < 0.05). While rhEpo‐treated animals were not initially protected from mechanical allodynia associated with L5 SNC, rhEpo did significantly improve recovery rates compared to vehicle‐treated animals (P < 0.01). Systemic rhEpo therapy increased JAK2 phosphorylation, a key anti‐apoptotic signalling molecule for Epo‐induced neuroprotection, in DRGs after crush. Dual immunofluorescence demonstrated Epo‐induced JAK2‐p was associated with both neuronal and glial cells. JAK2‐p was associated with NF200‐positive large neurons and with smaller neurons. This population of small neurons did not colocalize with IB4, a marker of nonpeptidergic, glial derived growth factor‐responsive neurons. The findings link anti‐apoptosis activities of Epo/EpoR/JAK2 in DRG neurons capable of inducing protracted pain states with reductions in pain behaviours, and therefore support a role for Epo therapy in the treatment of neuropathic pain.
Neuronal activity‐dependent increase of net matrix metalloproteinase activity is associated with MMP‐9 neurotoxicity after kainate
Authors: Jourquin Jérôme , Tremblay Evelyne , Décanis Nadège , Charton Gérard , Hanessian Stephen , Chollet Anne‐Marie , Le Diguardher Thierry , Khrestchatisky Michel , Rivera Santiago 
Published: September 2003

AbstractMatrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs) are emerging as important modulators of brain physiopathology. Dramatic changes in the expression of MMPs and TIMPs occur during excitotoxic/neuroinflammatory processes. However, only the measurement of net protease activity is relevant physiologically, and the functional consequences of MMP/TIMP ratio modifications in the brain remain elusive. In order to assess MMP activity and effects in brain tissue, we combinedin vivoand organotypic culture models of kainate (KA)‐induced excitotoxicity to provoke selective neuronal death and neuroinflammation in the hippocampus. Usingin situzymography, we show that KA‐induced excitotoxic seizures in rats increase net MMP activity in hippocampal neurons 8 h after seizures, before their death, and that this increase is neuronal activity‐dependent. Three days after KA, proteolytic activity increases in blood vessels and reactive glial cells of vulnerable areas, in relation with neuroinflammation. At 7 and 15 days, proteolysis remains high in blood vessels whereas it is reduced in glia. In organotypic hippocampal cultures, which lack blood cell‐mediated inflammation and extrinsic connections, a broad‐spectrum inhibitor of MMPs (MMPI), but also a selective MMP‐9 inhibitor, protect hippocampal neurons against KA‐induced excitotoxicity. Moreover, recombinant MMP‐9, but not MMP‐2, induces selective pyramidal cell death in these cultures and KA‐induced neuronal activity exacerbates the neuronal death promoting effects of MMP‐9. These data strongly implicate MMPs, and MMP‐9 in particular, in both excitotoxic neuronal damage and subsequent neuroinflammatory processes, and suggest that selective MMPIs could be therapeutically relevant in related neurological disorders.
Inhibition of neurokinin‐1–substance P receptor and prostanoid activity prevents and reverses the development of morphine tolerance in vivo and the morphine‐induced increase in CGRP expression in cultured dorsal root ganglion neurons
Authors: Powell Kelly J. , Quirion Remi , Jhamandas Khem 
Published: September 2003

AbstractChronic treatment with opioid drugs such as morphine leads to the development of tolerance, which manifests as a loss of drug potency. The mechanisms underlying this phenomenon are poorly understood, but recent evidence suggests that increased activity of nociceptive sensory transmitters [calcitonin gene‐related peptide (CGRP) and substance P] and other signalling messengers (prostaglandins) contribute to its development. Chronic intrathecal morphine administration to rats for 7 days produced analgesic tolerance. Co‐administration of SR140333, a selective substance P receptor (neurokinin‐1) antagonist, or nimesulide, a cyclooxygenase‐2‐selective inhibitor, augmented the acute effects of morphine, prevented morphine tolerance and reversed established tolerance. In cultured adult dorsal root ganglion neurons, exposure to morphine for 5 days increased the number of neurons expressing CGRP immunoreactivity. Co‐exposure with the peptide CGRP receptor antagonist CGRP8‐37, SR140333 or nimesulide prevented the morphine‐induced increase in the expression of CGRP immunoreactivity. Additionally, BIBN4096BS, a nonpeptide CGRP receptor antagonist, stereoselectively produced similar effects. In summary, this investigation demonstrates that activity of CGRP and substance P contributes to both the induction and expression of opioid analgesic tolerance. Additionally, it highlights the involvement of prostaglandins generated by spinal cyclooxygenase‐2 activity in the genesis of opioid tolerance. The neuropeptide and prostanoid activity contributing to tolerance is expressed at the level of the primary afferents terminating in the spinal cord. The combination of opioids with agents that block this activity may represent a useful strategy for the prevention as well as the reversal of clinical opioid tolerance.