bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultracytochemical Demonstration of Glycoproteins in the Eccrine Glands of the Digital Pads of the North American Raccoon (Procyon lotor)
Authors: Yasui T. , Tsukise A. , Meyer W. 
Published: January 2005

SummaryIn the eccrine glands of the digital pads of the North American raccoon (Procyon lotor), ultrastructural localization of glycoproteins with various saccharide residues was studied using preferably lectin cytochemical methods. Secretory granules observed in the dark cells exhibited glycoproteins with different terminal sugars (α‐d‐mannose, β‐d‐galactose, β‐N‐acetyl‐d‐glucosamine and sialic acid). The cytoplasm of the clear cells contained numerous glycogen particles. Several sugars were also detectable in the surface coat of the plasma membrane of the secretory cells. The results obtained could be helpful in understanding secretion production and cell related secretion functions of the eccrine glands of the raccoon digital foot pads.
The Role of Body Size in Mating Interactions of the Sexually Cannibalistic Fishing SpiderDolomedes triton
Authors: Johnson J. Chadwick 
Published: January 2005

AbstractSome arachnids display extreme sexual size dimorphism (SSD) with adult females being several times larger than adult males. One explanation for SSD in species that exhibit pre‐copulatory sexual cannibalism (female attack, kill and consumption of the male prior to mating) is that smaller males may be less likely victims of predatory attacks by females. However, in some sexually cannibalistic species SSD is relatively moderate (i.e. males are similar in size to females) suggesting benefits of large male body size. Here, I report the results of an experiment designed to explore the ramifications of body size in mating interactions of the sexually cannibalistic, North American fishing spider (Dolomedes triton). Results suggest that male size does not influence courtship behavior, the likelihood of being attacked, or the male's ability to secure a mounting. However, large males were superior at gaining copulations once mounted. Sexual cannibalism may also be predicated on female size. Female condition (mass/cephalothorax area) did not explain any of these behaviors from the copulatory sequence, however, females with a smaller cephalothorax area were more likely to attack courting males. Finally, analysis of the ratio of female size to male size showed that when SSD is weak males are more likely to escape attacks and mate successfully. Results are discussed in light of several hypotheses for sexual cannibalism, and the benefits of large male body size illustrated here are put forth as potential explanations for the relatively moderate extent of SSD found in this sexually cannibalistic species.
Mammalian isovalthine metabolism
Authors: Rutherfurd‐Markwick K. J. , Rogers Q. R. , Hendriks W. H. 
Published: January 2005

SummaryIsovalthine is a branched‐chain sulphur amino acid, which has been found in the urine of normal cats. The concentrations of isovalthine in the urine of healthy adult cats are approximately 24–66 μmol/l and are not affected by the gender of the cat. Isovalthinuria can be induced in other species (rats, rabbits, guinea‐pigs, humans, dogs) following the administration of certain inducing agents such as some hypocholesterolaemic agents, bile acids, hormones or cholesterol precursors. The method of induction of isovalthinuria was studied extensively during the 1960s, and efforts were made to understand its biosynthesis. However, although the origin of the sulphur atom in isovalthine was shown to be from cysteine or methionine, the origin of the carbon skeleton remains unknown. Interest in isovalthine metabolism was generated in part because it was reportedly found in the urine of patients with hypercholesterolaemia. The validity of this finding however, was brought into question following reports that administration of the drug Bromural (α‐bromoisovalerylurea), to humans results in the generation of compounds which break down to yield isovalthine following acid hydrolysis. This article presents a review and discussion of the experimental data on isovalthine metabolism.
Ascorbic acid concentrations in milk from Sudanese camels
Authors: Mohamed H. E. , Mousa H. M. , Beynen A. C. 
Published: January 2005

SummaryThe present study in Sudanese camels was done to describe the associations between vitamin C concentrations in milk, and either breed, stage of lactation, parity or the presence of mastitis. A total of 2586 camels were sampled. Arabi camels had higher ascorbic acid levels in milk than did either Anafi or Bishari camels. Milk ascorbic acid levels were higher for camels more than 180 days in lactation than for those earlier in lactation. Multiparous vs. primiparous camels had higher ascorbic acid concentrations in their milk. The ascorbic acid content of colostrum was higher than that of milk. Mastitis was associated with a decrease in the ascorbic acid content of both milk and blood plasma.
Respiratory infections during air travel
Authors: Leder K. , Newman D. 
Published: January 2005

AbstractAn increasing number of individuals undertake air travel annually. Issues regarding cabin air quality and the potential risks of transmission of respiratory infections during flight have been investigated and debated previously, but, with the advent of severe acute respiratory syndrome and influenza outbreaks, these issues have recently taken on heightened importance. Anecdotally, many people complain of respiratory symptoms following air travel. However, studies of ventilation systems and patient outcomes indicate the spread of pathogens during flight occurs rarely. In the present review, aspects of the aircraft cabin environment that affect the likelihood of transmission of respiratory pathogens on airplanes are outlined briefly and evidence for the occurrence of outbreaks of respiratory illness among airline passengers are reviewed. (Intern Med J 2005; 35: 50–55)
Modern management of portal hypertension
Authors: Lubel J. S. , Angus P. W. 
Published: January 2005

AbstractThe development of portal hypertension plays a major role in the pathogenesis of many of the complications of chronic liver disease. In developed countries, most patients with portal hypertension have cirrhosis, and, in this condition, portal pressure is elevated as a result of both an increase in hepatic resistance to portal perfusion and increased mesenteric blood flow. Bleeding from oesophageal varices is a major cause of mortality in patients with significant portal hypertension. This review concentrates on the recognition, prevention and acute management of this life threatening complication of cirrhosis. (Intern Med J 2005; 35: 45–49)
Outpatient treatment with subcutaneous interleukin‐2, interferon alpha and fluorouracil in patients with metastatic renal cancer: an Australian experience
Authors: Marx G. , Taylor J. , Goldstein D. 
Published: January 2005

AbstractBackground: Metastatic renal cell cancer has a poor prognosis and survival. Conventional cytotoxic chemotherapy has no impact on survival and response rates are low. Biologic agents are the most active in treating this disease. We report the feasibility of administering a combination of interferon alpha, subcutaneous interleukin‐2 and 5Fluorouracil in the outpatient setting to patients with metastatic renal cell cancer.Results: Between September 1996 and August 2003, fourteen patients were treated with this combination: ten males and four females with a median age of 50 (42–66). Thirteen patients had Eastern Cooperative Oncology Group performance scores of 0 or 1. Ten patients had had nephrectomies. Six patients had undergone prior treatments with chemotherapy or hormonal therapy. Twenty‐two cycles were administered (median 1, range of 1–4). Three patients achieved partial response, eight patients had stable disease, and three had progressive disease. The duration of response in patients with stable disease was (3, 3+, 4, 4+, 5+, 6, 10, 11 months) and for the patients with a partial response was 2+, 11 and 12 months. Toxicities with this combination were predictable. There were no treatment‐related deaths and no episodes of febrile neutropenia. One patient ceased treatment as a result of toxicity. Fatigue was the most common side‐effect. Myalgias, fever and rigors occurred within 6–12 h of administration of interleukin‐2, and resolved within 12 h. Grade 1–2 nausea and vomiting occurred in most patients. Four patients had transient asymptomatic transaminitis, which resolved spontaneously. As a result of toxicity, one patient had treatment ceased in his 6th week.Conclusion: This combination was feasible, well tolerated and manageable in an outpatient setting. (Intern Med J 2005; 35: 34–38)
A Random Variable Related to the Inversion Vector of a Partial Random Permutation
Authors: Laghate Kavita , Deshpande M. N. 
Published: January 2005

SummaryIn this article, we define the inversion vector of a permutation of the integers 1, 2, . . . , n. We set up a particular kind of permutation, called a partial random permutation. The sum of the elements of the inversion vector of such a permutation is a random variable of interest.
Neuronal death in primary retinal cultures is related to nitric oxide production, and is inhibited by erythropoietin in a glucose‐sensitive manner
Authors: Layton C. J. , Wood J. P. M. , Chidlow G. , Osborne N. N. 
Published: January 2005

AbstractThe aim of this work was to investigate the interrelated effects of glucose, nitric oxide (NO) and erythropoietin on neuronal survival in retinal cultures, thereby exploring the mechanism of neuronal death in the diabetic retina. Rat retinal cells were cultured in low (5 mm) or high (15 mm) glucose concentrations. After 9 days, cell viability was assessed by (3,4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT) assay and NO production was determined by the Griess reaction. Immunohistochemistry was used to quantify GABA‐labelled neurones and cells staining for DNA breakdown. High or low glucose concentrations had no effect on basal NO production or the survival of neurones in culture, but treatment with N‐nitro‐l‐arginine methyl ester reduced extracellular levels of NO and increased neuronal survival at both concentrations of glucose. Erythropoietin decreased cell death and NO levels, but only in cultures grown in low concentrations of glucose. It is concluded that erythropoietin's neurotrophic function in the retina is attenuated at glucose concentrations similar to those which occur in diabetes.
AG490 prevents cell death after exposure of rat astrocytes to hydrogen peroxide or proinflammatory cytokines: involvement of the Jak2/STAT pathway
Authors: Gorina Roser , Petegnief Valérie , Chamorro Ángel , Planas Anna M. 
Published: January 2005

AbstractJanus kinases/STAT pathway mediates cellular responses to certain oxidative stress stimuli and cytokines. Here we examine the activation of Stat1 and Stat3 in rat astrocyte cultures and its involvement in cell death. H2O2, interferon (INF)‐γ and interleukin (IL)‐6 but not IL‐10 caused cell death. Stat1 was phosphorylated on tyrosine (Tyr)‐701 after exposure to H2O2, INF‐γ or IL‐6 but not IL‐10. Tyr‐705 pStat3 was observed after H2O2, IL‐6 and IL‐10. Also, H2O2induced serine (Ser)‐727 phosphorylation of Stat1 but not Stat3. The degree of Tyr‐701 pStat1 by the different treatments positively correlated with the corresponding reduction of cell viability. AG490, a Jak2 inhibitor, prevented Tyr‐701 but not Ser‐727, Stat1 phosphorylation. Also, AG490 inhibited Tyr‐705 Stat3 phosphorylation induced by H2O2and IL‐6 but did not prevent that induced by IL‐10. Furthermore, AG490 conferred strong protection against cell death induced by INF‐γ, IL‐6 and H2O2. These results suggest that Jak2/Stat1 activation mediates cell death induced by proinflammatory cytokines and peroxides. However, we found evidence suggesting that AG490 reduces oxidative stress induced by H2O2, which further shows that H2O2and/or derived reactive oxygen species directly activate Jak2/Stat1, but masks the actual involvement of this pathway in H2O2‐induced cell death.
Bi‐functional effects of ATP/P2 receptor activation on tumor necrosis factor‐alpha release in lipopolysaccharide‐stimulated astrocytes
Authors: Kucher Brandon M. , Neary Joseph T. 
Published: January 2005

AbstractNeuroinflammation is associated with a variety of CNS pathologies. Levels of tumor necrosis factor‐alpha (TNF‐α), a major proinflammatory cytokine, as well as extracellular ATP, are increased following various CNS insults. Here we report on the relationship between ATP/P2 purinergic receptor activation and lipopolysaccharide (LPS)‐induced TNF‐α release from primary cultures of rat cortical astrocytes. Using ELISA, we confirmed that treatment with LPS stimulated the release of TNF‐α in a concentration and time dependent manner. ATP treatment alone had no effect on TNF‐α release. LPS‐induced TNF‐α release was attenuated by 1 mm ATP, a concentration known to activate P2X7 receptors. Consistent with this, 3′‐O‐(4‐Benzoyl)benzoyl‐ATP (BzATP), a P2X7 receptor agonist, also attenuated LPS‐induced TNF‐α release. This reduction in TNF‐α release was not due to loss of cell viability. Adenosine and 2‐chloroadenosine were ineffective, suggesting that attenuation of LPS‐induced TNF‐α release by ATP was not due to ATP breakdown and subsequent activation of adenosine/P1 receptors. Interestingly, treatment of astrocyte cultures with 10 µm or 100 µm ATP potentiated TNF‐α release induced by a submaximal concentration of LPS. UTP and 2methylthioADP (2‐MeSADP), P2Y receptor agonists, also enhanced this LPS‐induced TNF‐α release. Our observations demonstrate opposing effects of ATP/P2 receptor activation on TNF‐α release, i.e. P2X receptor activation attenuates, whereas P2Y receptor activation potentiates TNF‐α release in LPS‐stimulated astrocytes. These observations suggest a mechanism whereby astrocytes can sense the severity of damage in the CNS via ATP release from damaged cells and can modulate the TNF‐α mediated inflammatory response depending on the extracellular ATP concentration and corresponding type of astrocyte ATP/P2 receptor activated.
Co‐localization and functional interaction between adenosine A2A and metabotropic group 5 receptors in glutamatergic nerve terminals of the rat striatum
Authors: Rodrigues Ricardo J. , Alfaro Tiago M. , Rebola Nelson , Oliveira Catarina R. , Cunha Rodrigo A. 
Published: January 2005

AbstractThe anti‐Parkinsonian effect of glutamate metabotropic group 5 (mGluR5) and adenosine A2A receptor antagonists is believed to result from their ability to postsynaptically control the responsiveness of the indirect pathway that is hyperfunctioning in Parkinson's disease. mGluR5 and A2A antagonists are also neuroprotective in brain injury models involving glutamate excitotoxicity. Thus, we hypothesized that the anti‐Parkinsonian and neuroprotective effects of A2A and mGluR5 receptors might be related to their control of striatal glutamate release that actually triggers the indirect pathway. The A2A agonist, CGS21680 (1–30 nm) facilitated glutamate release from striatal nerve terminals up to 57%, an effect prevented by the A2A antagonist, SCH58261 (50 nm). The mGluR5 agonist, CHPG (300–600 μm) also facilitated glutamate release up to 29%, an effect prevented by the mGluR5 antagonist, MPEP (10 μm). Both mGluR5 and A2A receptors were located in the active zone and 57 ± 6% of striatal glutamatergic nerve terminals possessed both A2A and mGluR5 receptors, suggesting a presynaptic functional interaction. Indeed, submaximal concentrations of CGS21680 (1 nm) and CHPG (100 μm) synergistically facilitated glutamate release and the facilitation of glutamate release by 10 nm CGS21680 was prevented by 10 μm MPEP, whereas facilitation by 300 μm CHPG was prevented by 10 nm SCH58261. These results provide the first direct evidence that A2A and mGluR5 receptors are co‐located in more than half of the striatal glutamatergic terminals where they facilitate glutamate release in a synergistic manner. This emphasizes the role of the modulation of glutamate release as a likely mechanism of action of these receptors both in striatal neuroprotection and in Parkinson's disease.
Anesthesia and post‐mortem interval profoundly influence the regulatory serine phosphorylation of glycogen synthase kinase‐3 in mouse brain
Authors: Li Xiaohua , Friedman Ari B. , Roh Myoung‐Sun , Jope Richard S. 
Published: January 2005

AbstractGlycogen synthase kinase‐3 (GSK3) is a crucial enzyme contributing to the regulation of neuronal structure, plasticity and survival, is implicated as a contributory factor in prevalent diseases such as Alzheimer's disease and mood disorders and is regulated by a wide range of signaling systems and pharmacological agents. Therefore, factors regulating GSK3 in vivo are currently of much interest. GSK3 is inhibited by phosphorylation of serine‐9 or serine‐21 in GSK3β and GSK3α, respectively. This study found that accurate measurements of phospho‐Ser‐GSK3 in brain are confounded by a rapid post‐mortem dephosphorylation, with ∼90% dephosphorylation of both GSK3 isoforms occurring within 2 min post‐mortem. Furthermore, three anesthetics, pentobarbital, halothane and chloral hydrate, each caused large in vivo increases in the serine phosphorylation of both GSK3β and GSK3α in several regions of mouse brain. Thus, studies of the phosphorylation state of GSK3 in brain, and perhaps in other tissues, need to take into account post‐mortem changes and the effects of anesthetics and there is a direct correlation between anesthesia and high levels of serine‐phosphorylated GSK3.
BAALC 1‐6‐8 protein is targeted to postsynaptic lipid rafts by its N‐terminal myristoylation and palmitoylation, and interacts with α, but not β, subunit of Ca2+/calmodulin‐dependent protein kinase II
Authors: Wang Xin , Tian Qing‐Bao , Okano Akira , Sakagami Hiroyuki , Moon Il Soo , Kondo Hisatake , Endo Shogo , Suzuki Tatsuo 
Published: January 2005

AbstractWe cloned a rat BAALC 1‐6‐8 isoform cDNA (GenBank™ Accession No. AB073318) that encoded a 22‐kDa protein, and identified endogenous BAALC 1‐6‐8 protein in the brain. The gene was expressed widely in the frontal part of the brain, and the protein was localized to the synaptic sites and was increased in parallel with synaptogenesis. The protein interacted with the α, but not β, subunit of Ca2+/calmodulin‐dependent protein kinase II (CaMKIIα). The interaction occurred between the N‐terminal 35‐amino‐acid region of BAALC 1‐6‐8 protein and the C‐terminal end of the regulatory domain of CaMKIIα, which contains α isoform‐specific sequence. Thus, the interaction may be CaMKIIα‐specific. We also found that BAALC 1‐6‐8 protein, as well as CaMKIIα, was localized to lipid rafts and that both myristoylation and palmitoylation of BAALC 1‐6‐8 N‐terminal portion were required for targeting of the protein into lipid rafts. These findings suggest that BAALC 1‐6‐8 protein play a synaptic role at the postsynaptic lipid raft possibly through interaction with CaMKIIα.
Brain‐derived neurotrophic factor prevents changes in Bcl‐2 family members and caspase‐3 activation induced by excitotoxicity in the striatum
Authors: Pérez‐Navarro Esther , Gavaldà Núria , Gratacòs Elena , Alberch Jordi 
Published: January 2005

AbstractBrain‐derived neurotrophic factor (BDNF) prevents the loss of striatal neurons caused by excitotoxicity. We examined whether these neuroprotective effects are mediated by changes in the regulation of Bcl‐2 family members. We first analyzed the involvement of the phosphatidylinositol 3‐kinase/Akt pathway in this regulation, showing a reduction in phosphorylated Akt (p‐Akt) levels after both quinolinate (QUIN, an NMDA receptor agonist) and kainate (KA, a non‐NMDA receptor agonist) intrastriatal injection. Our results also show that Bcl‐2, Bcl‐xL and Bax protein levels and heterodimerization are selectively regulated by NMDA and non‐NMDA receptor stimulation. Striatal cell death induced by QUIN is mediated by an increase in Bax and a decrease in Bcl‐2 protein levels, leading to reduced levels of Bax:Bcl‐2 heterodimers. In contrast, changes in Bax protein levels are not required for KA‐induced apoptotic cell death, but decreased levels of both Bax:Bcl‐2 and Bax:Bcl‐xL heterodimer levels are necessary. Furthermore, QUIN and KA injection activated caspase‐3. Intrastriatal grafting of a BDNF‐secreting cell line counter‐regulated p‐AKT, Bcl‐2, Bcl‐xL and Bax protein levels, prevented changes in the heterodimerization between Bax and pro‐survival proteins, and blocked caspase‐3 activation induced by excitotoxicity. These results provide a possible mechanism to explain the anti‐apoptotic effect of BDNF against to excitotoxicity in the striatum through the regulation of Bcl‐2 family members, which is probably mediated by Akt activation.
S100B‐induced microglial and neuronal IL‐1 expression is mediated by cell type‐specific transcription factors
Authors: Liu Ling , Li Yuekui , Van Eldik Linda J. , Griffin W. Sue T. , Barger Steven W. 
Published: January 2005

AbstractBoth the astrocytic cytokine S100B and the pro‐inflammatory interleukin‐1 (IL‐1) are elevated in Alzheimer's disease, and each has been implicated in Alzheimer‐related neuropathology. We examined the gene‐regulatory events through which S100B induces IL‐1β expression. In primary microglia, S100B activated the transcription factors Sp1 and NFκB, followed by an increase in IL‐1β mRNA levels. The latter was blocked by a peptide inhibitor of NFκB or by a double‐stranded oligonucleotide containing a NFκB‐binding site to serve as ‘decoy’ DNA and reduce available NFκB. But in primary cortical neurons, decoy and siRNA experiments indicated that the IL‐1β induction by S100B was mediated by Sp1 without evidence of a role for NFκB. Our results suggest that the elevation of S100B and IL‐1 in Alzheimer brain and consequent neurodegenerative events are mediated through cell‐type specific gene‐regulatory events, providing mechanistic insight into connections between glial activation and neuronal dysfunction.
Effects of brain‐derived neurotrophic factor (BDNF) on glial cells and serotonergic neurones during development
Authors: Djalali S. , Höltje M. , Große G. , Rothe T. , Stroh T. , Große J. , Deng D. R. , Hellweg R. , Grantyn R. , Hörtnagl H. , Ahnert‐Hilger G. 
Published: January 2005

AbstractSerotonergic neurones are among the first to develop in the central nervous system. Their survival and maturation is promoted by a variety of factors, including serotonin itself, brain‐derived neurotrophic factor (BDNF) and S100β, an astrocyte‐specific Ca2+ binding protein. Here, we used BDNF‐deficient mice and cell cultures of embryonic raphe neurones to determine whether or not BDNF effects on developing serotonergic raphe neurones are influenced by its action on glial cells. In BDNF–/– mice, the number of serotonin‐immunoreactive neuronal somata, the amount of the serotonin transporter, the serotonin content in the striatum and the hippocampus, and the content of 5‐hydroxyindoleacetic acid in all brain regions analysed were increased. By contrast, reduced immunoreactivity was found for myelin basic protein (MBP) in all brain areas including the raphe and its target region, the hippocampus. Exogenously applied BDNF increased the number of MBP‐immunopositive cells in the respective culture systems. The raphe area displayed selectively reduced immunoreactivity for S100β. Accordingly, S100β was increased in primary cultures of pure astrocytes by exogenous BDNF. In glia‐free neuronal cultures prepared from the embryonic mouse raphe, addition of BDNF supported the survival of serotonergic neurones and increased the number of axon collaterals and primary dendrites. The latter effect was inhibited by the simultaneous addition of S100β. These results suggest that the presence of BDNF is not a requirement for the survival and maturation of serotonergic neurones in vivo. BDNF is, however, required for the local expression of S100β and production of MBP. Therefore BDNF might indirectly influence the development of the serotonergic system by stimulating the expression of S100β in astrocytes and the production MBP in oligodendrocytes.