bluuebunny/crossref_metadata_2025_split huggingface dataset:
Constant Light Exposure Causes Dissociation in Gonadotrophin Secretion and Inhibits Partially Neuroendocrine Differentiation of Leydig Cells in Adult Rats
Authors: Ortega HH , Lorente JA , Mira GA , Baravalle C , Salvetti NR 
Published: December 2004

ContentsThe objective of this work was to study the changes that occur in the Leydig cells of rats exposed to continuous light. The laboratory rat is considered a non‐photoperiodic species because exposure to short photoperiod has little or no effect on the reproductive status. However, exposure of adult female rats to constant light induces polycystic ovaries, indicating that extreme changes in the photoperiod affect the reproductive function seriously. Adult male rats were placed under continuous light conditions for a duration of 15 weeks. After this period, the animals were killed and testicles were dissected and processed by routine histologic protocols. Follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) serum levels were determined by radioimmunoassay (RIA). The visualization of antigens was achieved by the streptavidin‐peroxidase immunohistochemical method. Antibodies against chromogranin A, S‐100 protein, P substance, synaptofisin, neurofilament protein‐200, gliofibrillary acidic protein and neurone‐specific enolase were used. The mean LH serum concentration was significantly lower, while the mean FSH level was significantly higher in treated animals. The expression of S‐100, NSE, CrA, SP and SYN was significantly lower in treated animals. In conclusion, the constant light exposure acting directly at the pituitary level decreases LH secretion. The increased FSH secretion may be due to a partial reduction of the negative androgen feedback in the pituitary gland. Moreover, the constant light exposure affects the expression of some immunomarkers in Leydig cells, possibly because of the changes found in the gonadotrophin level and feedback mechanism.
Different Culture Media Requirements of IVF and Nuclear Transfer Bovine Embryos
Authors: Mastromonaco GF , Semple E , Robert C , Rho GJ , Betts DH , King WA 
Published: December 2004

ContentsImportant differences exist between in vitro fertilized (IVF) and nuclear transfer (NT) bovine embryos. Studies have shown that although in vitro development is comparable, post‐implantation survival is greatly reduced in NT embryos. In this study, we compare serum and bovine serum albumin (BSA) supplementation during oocyte maturation and embryo culture of IVF and NT embryos. In experiment 1, oocytes and embryos were randomly distributed into different treatment groups consisting of synthetic oviductal fluid (SOF) medium supplemented with either serum, fatty acid‐free BSA (FAF) or fraction V BSA during maturation and/or culture to assess IVF embryo development. In experiment 2, oocytes were matured in SOF + serum or SOF + FAF and reconstructed embryos were cultured in SOF + FAF to assess NT embryo development. Among the IVF treatment groups, a greater number of blastocysts were observed in the steer serum (SER) group (IVM and IVC in SOF + serum) on day 6; however, no significant differences were seen in blastocyst development from day 8 onwards. Hatching frequencies on days 8 and 9 were significantly greater in groups with serum, with the exception of FAF (IVM and IVC in SOF + FAF) on day 9. For the NT treatment groups, the presence of serum during IVM resulted in a higher proportion of MII oocytes and increased blastocyst development and hatching rates were compared with supplementation of FAF. These results indicate that both serum and FAF provide comparable embryo development for IVF but not for NT bovine embryos.
Liver abscess in inflammatory bowel disease: Report of two cases and review of the literature
Authors: MARGALIT MAYA , ELINAV HILA , ILAN YARON , SHALIT MEIR 
Published: December 2004

AbstractHepatic abscesses are a rare complication of inflammatory bowel disease (IBD). Despite the fact that certain hepatobiliary complications of IBD, including cholelithiasis, primary sclerosing cholangitis (PSC) and cholangiocarcinoma predispose patients with IBD to ascending cholangitis, previously published data does not demonstrate that biliary infection is an important mechanism underlying liver abscess development in these patients. We describe two patients with inflammatory bowel disease, both with PSC, who developed multiple liver abscesses, and review the literature on liver abscesses in association with inflammatory bowel disease.© 2004 Blackwell Publishing Asia Pty Ltd
Utilization of eye care services by Victorians likely to benefit from eye care
Authors: Bylsma Guy W , Le Anhchuong , Mukesh Bickol N , Taylor Hugh R , McCarty Catherine A 
Published: December 2004

Abstract Aim: To assess the utilization of eye care services by Australians most likely to benefit from eye assessment. Methods: The Melbourne Visual Impairment Project was a population‐based study that collected demographic, health and vision‐related information including use of eye care services. A standardized detailed ophthalmic examination was performed. Utilization of eye care services by those who might most benefit from eye care was assessed and compared to the general population. These participants include those with undiagnosed glaucoma, unoperated visually significant cataract, undercorrected refractive error, diabetes mellitus, age‐related macular degeneration and visual acuity < 6/12. Sociodemographic characteristics were assessed for their influence on eye care utilization among these participants. Results: A total of 4744 urban and rural residents participated (86% of those eligible) and 4612 (83% of total eligible) of these had a complete data set for the use of eye care services and were included. There were 933 participants (20.2%) who did not report eye assessment in the previous 5 years, and 891 participants (19.3%) had one or more aforementioned conditions potentially benefiting from eye care. Of these, between 34.4% and 59.4% reported no examination in the previous year and between 9% and 25% reported no examination within the previous 5 years. These participants were more likely to seek eye care within the short term (1 year) if they had a family history of eye disease, otherwise a noticed change in vision was the main influence in the longer term (2–5 years). Male participants, younger participants and those whose main spoken language was not English were less likely to seek eye care in the longer term. Conclusions: In Victoria 19% of those >40 years of age have potentially unmanaged eye disease including glaucoma, unoperated visually significant cataract, undercorrected refractive error, age‐related macular degeneration, diabetes mellitus or visual acuity < 6/12. A substantial proportion of these report no eye assessment in the previous 1, 2 or 5 years or ever before. Younger age, male sex and main language other than English make assessment less likely. Many may have these conditions despite having had a recent eye assessment.
Analysis of symptoms associated with rhegmatogenous retinal detachments
Authors: Polkinghorne Philip J , Craig Jennifer P 
Published: December 2004

AbstractAim: The symptoms associated with rhegmatogenous retinal detachments are variable and can be associated with other vitreoretinal and neuro‐ophthalmic entities. The present study sought to determine the frequency and type of symptoms associated with rhegmatogenous retinal detachment (RRD), and analyse any relationships with the premorbid state.Methods: An observational case series was undertaken. A patient questionnaire together with clinical data was collected for patients presenting with RRD.Results: The data on 141 patients presenting with RRD were evaluated prospectively. More than 90% of patients reported a variety of symptoms including visual loss, floaters and flashes. The speed of visual loss was not associated with the extent of retinal break. Rather unexpectedly, patients with a history of retinal pathology were not any more likely to be symptomatic either in their presenting or fellow eye. The absence of symptoms was not associated with age, high myopia or previous cataract surgery.Conclusion: Both patients and physicians need to be aware of the importance of the symptoms associated with RRD.
New vehicle based on a microemulsion for topical ocular administration of dexamethasone
Authors: Fialho Sílvia Ligório , Da Silva‐Cunha Armando 
Published: December 2004

AbstractAim: Eye drops are the most used dosage form by the ocular route, in spite of their low bioavailability. Due to their properties and numerous advantages, microemulsions are promising systems for topical ocular drug delivery. They can increase water solubility of the drug and enhance drug absorption into the eye. The present study describes the development and characterization of an oil‐in‐water microemulsion containing dexamethasone and the evaluation of its pharmacokinetics in rabbits after topical ocular application.Methods: The microemulsion was prepared by the titration technique. Its physico‐chemical characteristics and stability were determined. The ocular irritation test and the pharmacokinetics of this system were studied in white rabbits.Results: The developed system showed an acceptable physico‐chemical behaviour and presented good stability for 3 months. The ocular irritation test used suggested that the microemulsion did not provide significant alteration to eyelids, conjunctiva, cornea and iris. This formulation showed greater penetration of dexamethasone in the anterior segment of the eye and also release of the drug for a longer time when compared with a conventional preparation. The area under the curve obtained for the microemulsion system was more than twofold higher than that of the conventional preparation (P < 0.05).Conclusions: The microemulsion‐based dexamethasone eye drop is advantageous for ophthalmic use because it is well‐tolerated in the eye and seemed to provide a higher degree of bioavailability. The developed system shows greater penetration in the eye, allowing the possibility of decreasing the number of applications of eye drops per day.
Reduced food anticipatory activity in genetically orexin (hypocretin) neuron‐ablated mice
Authors: Akiyama Masashi , Yuasa Tomoyo , Hayasaka Naomi , Horikawa Kazumasa , Sakurai Takeshi , Shibata Shigenobu 
Published: December 2004

AbstractDaily restricted feeding (RF) produces an anticipatory locomotor activity rhythm and entrains the peripheral molecular oscillator independently of the central pacemaker located in the suprachiasmatic nucleus (SCN). As orexins (hypocretins) are neuropeptides that coordinate sleep/wake patterns and motivated behaviours, such as food seeking, we studied the involvement of orexin in the food anticipatory activity (FAA) induced by RF. Daily RF shifted the mRNA rhythm of a clock‐controlled gene mDbp in the cerebral cortex and caudate putamen but not in the SCN. Under these experimental conditions, prepro‐orexin mRNA and orexin A immunoreactivity in the lateral hypothalamic area (LHA) did not show daily variation. Fasting increased the number of orexin A‐ir cells, while RF did not. However, RF shifted the peak of Fos expression of the orexin neurons from night to day. Genetic ablation of orexin neurons in orexin/ataxin‐3 transgenic mice severely reduced the formation of FAA under RF conditions. The expression of mNpas2 mRNA, a transcription factor thought to be involved in regulation of the food entrainable oscillator as well as mPer1 and mBmal1 mRNA, was reduced in the forebrain of orexin/ataxin‐3 mice. Based on these results, we suggest that activity of the orexin neuron in the LHA contributes to the promotion and maintenance of FAA.
Caspase signalling in neuropathic and inflammatory pain in the rat
Authors: Joseph Elizabeth K. , Levine Jon D. 
Published: December 2004

AbstractWhereas small‐fibre sensory neuropathies might ultimately lead to cell death and loss of sensation, they first progress through a phase, which might last for years, characterized by the presence of analgesia‐resistant neuropathic dysesthesias and pain. Much previous research has addressed these two phases as separate phenomena mediated by presumably discrete biochemical mechanisms. We hypothesized that activity in signalling pathways that ultimately lead to apoptosis plays a critical role in the generation of neuropathic pain, before death of sensory neurons becomes apparent. We have tested the hypothesis that activator and effector caspases, defining components of programmed cell death (apoptosis) signalling pathways, also contribute to pain‐related behaviour in animals with small‐fibre peripheral neuropathies and that the death receptor ligand, tumour necrosis factor‐α, and its downstream second messenger, ceramide, also produce pain‐related behaviour via this mechanism. In two models of painful peripheral neuropathy, HIV/AIDS therapy (induced by the nucleoside reverse transcriptase inhibitor, dideoxycytidine), and cancer chemotherapy (induced by vincristine) peripheral neuropathy, and for pain‐related behaviour induced by tumour necrosis factor‐α and its second messenger, ceramide, inhibition of both activator (1, 2, 8 and 9) and effector (3) caspases attenuates neuropathic pain‐related behaviour, although has no effect in streptozotocin‐diabetic neuropathy and control rats. We conclude that during a latent phase, before apoptotic cell death is manifest, the caspase signalling pathway can contribute to pain in small‐fibre peripheral neuropathies, and that inflammatory/immune mediators also activate these pathways. This suggests that these pathways are potential targets for novel pharmacological agents for the treatment of inflammatory as well as neuropathic pain.
Differential activation of MAPK in injured and uninjured DRG neurons following chronic constriction injury of the sciatic nerve in rats
Authors: Obata Koichi , Yamanaka Hiroki , Dai Yi , Mizushima Toshiyuki , Fukuoka Tetsuo , Tokunaga Atsushi , Noguchi Koichi 
Published: December 2004

AbstractTo investigate the intracellular signal transduction pathways involved in the pathophysiological mechanisms of neuropathic pain after partial nerve injury, we examined the activation of extracellular signal‐regulated protein kinase (ERK) and p38 mitogen‐activated protein kinase (MAPK) in the dorsal root ganglion (DRG) in the chronic constriction injury (CCI) model. The CCI induced an increase in the phosphorylation of ERK in predominantly injured medium‐sized and large‐sized DRG neurons and in satellite glial cells. Treatment with the MAPK kinase 1/2 inhibitor, U0126, suppressed CCI‐induced mechanical allodynia and partially reversed the increase in neuropeptide Y (NPY) expression in damaged DRG neurons. In contrast, the CCI induced the activation of p38, mainly in uninjured small‐to‐medium‐diameter DRG neurons and in satellite glial cells. The p38 inhibitor, SB203580, reversed the CCI‐induced heat hyperalgesia and also the increase in brain‐derived neurotrophic factor (BDNF) expression in intact DRG neurons. On the other hand, the nerve growth factor (NGF)‐induced increase in BDNF expression in small‐to‐medium‐diameter neurons was reversed by SB203580, whereas the anti‐NGF‐induced increase in NPY in medium‐sized and large‐sized neurons was partially blocked by U0126. Taken together, our results demonstrate that the activation of ERK and p38 and also the changes in NPY and BDNF expression may occur in different populations of DRG neurons after CCI, partially through alterations in the target‐derived NGF. These changes in injured and intact primary afferents are likely to have a substantial role in pathological states, and MAPK pathways in nociceptors may be potential targets for the development of novel analgesics.
Rt‐PA causes a significant increase in endogenous u‐PA during experimental focal cerebral ischemia
Authors: Burggraf Dorothe , Martens Helge K. , Wunderlich Nathalie , Jäger Gabriele , Hamann Gerhard F. 
Published: December 2004

AbstractThe aim of this study was to investigate the effects of different doses of exogenous recombinant human tissue plasminogen activator (rt‐PA) on the endogenous cerebral plasminogen–plasmin system in focal ischemia in rats. Ischemia was induced using the suture model. Each group of rats (n = 6) received either treatment (0.9, 9 or 18 mg rt‐PA/kg body weight) or saline (control group) at the end of ischemia; a sham‐operated group was added. The activity of the plasminogen activators was measured by casein‐dependent plasminogen zymography. In the cortex urokinase (u‐PA) rose from sham (no ischemia), 91 ± 7% to ischemia, 176 ± 10% (P < 0.005). Increasing rt‐PA doses led to further significant (P < 0.001) cortical u‐PA activation which was maximal at 18 mg: 249 ± 13%. An extreme increase in the u‐PA activity was observed in the basal ganglia to 1019 ± 22% (P < 0.001). This increase was further aggravated by higher rt‐PA doses (18 mg, 1236 ± 15%; P < 0.001). The t‐PA level did not change I3R24 during (3 h ischemia followed by reperfusion for 24 h); however, during low and moderate doses of rt‐PA, endogenous t‐PA was reduced. In conclusion, while ischemia leads to a significant increase in u‐PA, mainly in the basal ganglia, t‐PA is not altered. Increasing doses of rt‐PA lead to a further elevation of u‐PA. Thus, u‐PA seems to play a major role in the endogenous plasminogen activator system following focal cerebral ischemia.
GABA‐immunoreactive starburst amacrine cells in pigmented and albino rats
Authors: Blaszczyk W. M. , Telkes I. , Distler C. 
Published: December 2004

AbstractIn this study we tested whether the critical anatomical substrate for retinal direction selectivity is altered in albino mammals. We used dual immunostaining for GABA and choline acetyltransferase and quantitatively analyzed the number of double‐labelled starburst amacrine cells in wild‐type and albino rats. In albino rats, the percentage of ON‐amacrine cells with high GABA content was significantly lower than in pigmented animals. OFF‐amacrines did not significantly differ between the two rat strains. Thus, the decreased GABA content in ON‐amacrine cells could reflect an altered neuronal substrate for retinal direction selectivity. These results are discussed in relation to the optokinetic deficits described in albino mammals.
Effects of ventral hippocampal lesion on thermal and mechanical nociception in neonates and adult rats
Authors: Al Amin Hassen A. , Atweh Samir F. , Jabbur Suhayl J. , Saadé Nayef E. 
Published: December 2004

AbstractThe proper maturation of the hippocampus is essential for the development of different behaviours, including memory, pain responses and avoidance. The mechanisms involved in the neurodevelopment of nociception have also been implicated in several neuropsychiatric disorders. The neonatal lesion of the ventral hippocampus (VH) in rats, an animal model of schizophrenia, can be utilized to study the developmental neurobiology of animal behaviour. We examined the nociceptive responses in this animal model at different stages of development. Rat pups were lesioned at postnatal day 7 by injecting ibotenic acid into the VH bilaterally, and then tested for thermal and mechanical nociception at the age of 35, 65 and 180 days. The nociceptive tests used were the hot plate (HP), paw pressure (PP) and tail flick (TF) tests. Another group of adult rats had the same lesion in the VH and then underwent the same tests at 28, 56 and 168 days post‐lesions. When compared with sham controls, the rats with neonatal VH lesion showed decreased latency for the HP and PP tests only after puberty. The TF test showed significant increase in latency for both groups at age 65 and 180 days. The adult rats with VH lesion showed no major changes over all periods of testing. These results suggest that early lesion of VH can alter the development of the neural mechanisms involved in the processing of thermal and mechanical nociception.
Fez1 is layer‐specifically expressed in the adult mouse neocortex
Authors: Inoue Kiyoshi , Terashima Toshio , Nishikawa Toru , Takumi Toru 
Published: December 2004

AbstractThe mammalian cerebral neocortex occupies the largest area of the cerebral cortex and is cytoarchitectually composed of six layers (I–VI). Recent molecular analysis has begun to reveal the existence of various developmental programs, including the genetic regulation of arealization of the neocortex. Although an increasing number of molecular determinants of the developmental stages of the neocortex have been identified, no genes specifically expressed in the adult neocortex have been identified to date. By global screening using microarrays, combined with systematic in situ hybridization, we identified a zinc‐finger type transcription factor, Fez1, which is expressed predominantly in the mouse adult neocortex. No other genes in the neocortex have been shown to date to have their expression with such high specificity. Using two‐color in situ hybridization, we show that Fez1 is mainly expressed in cortical layers V and VI, not in γ‐aminobutyric acid neurons but in pyramidal neurons, the projection neurons of the cerebral cortex. Immunohistochemistry also shows that Fez1 is expressed in deep layers of the neocortex. Fez1 will be invaluable not only for the molecular understanding of corticogenesis but also for understanding the physiological functions of the adult neocortex, as well as for the use of its promoter in gene‐manipulated animals and in conditional expression systems.
Benefit of valproic acid in suppressing disease progression of ALS model mice
Authors: Sugai Fuminobu , Yamamoto Yoichi , Miyaguchi Katsuyuki , Zhou Zhiwei , Sumi Hisae , Hamasaki Toshimitsu , Goto Masashi , Sakoda Saburo 
Published: December 2004

AbstractValproic acid (VPA) has long been used as an antiepileptic drug and recently as a mood stabilizer, and evidence is increasing that VPA exerts neuroprotective effects through changes in a variety of intracellular signalling pathways including upregulation of Bcl‐2 protein with an antiapoptotic property and inhibiting glycogen synthase kinase 3‐β, which is considered to promote cell survival. Although the neuroprotective effects of VPA have been demonstrated in a murine model of human immunodeficiency virus‐1 encephalitis, there have been no reports on the effect of VPA in chronic progressing neurodegenerative disease models including amyotrophic lateral sclerosis (ALS). ALS is a devastating disease selectively affecting motoneurons, and its disease model mice bear a close resemblance to ALS symptomatically and pathologically. First, we used an organotypic slice culture using mouse spinal cord, and showed that VPA protected spinal motoneurons against death from glutamate toxicity in vitro. Then, we treated ALS model mice with VPA at the dose effective level for epileptic model mice after 45 days of age (pre‐onset treatment) or the day of the disease onset (post‐onset treatment). We found a significant prolongation of the disease duration in ALS model mice in both methods of treatment. Considering the long usage of VPA for epileptic patients with good tolerance and safety, these data strongly support the clinical application of VPA for ALS treatment.