bluuebunny/crossref_metadata_2025_split huggingface dataset:
Observations on the histochemistry and ultrastructure of the epidermis of the tuatara, Sphenodon punctatus (Sphenodontida, Lepidosauria, Reptilia): A contribution to an understanding of the lepidosaurian epidermal generation and the evolutionary origin of the squamate shedding complex
Authors: Alibardi Lorenzo , Maderson Paul F.A. 
Published: March 2003

AbstractHistochemical and TEM analysis of the epidermis of Sphenodon punctatus confirms previous histological studies showing that skin‐shedding in this relic species involves the periodic production and loss of epidermal generations, as has been well documented in the related Squamata. The generations are basically similar to those that have been described in the latter, and their formation involves a cyclic alternation between β‐ and α‐keratogenesis. The six differences from the previously described squamate condition revealed by this study include: 1) the absence of a well‐defined shedding complex; 2) the persistence of plasma membranes throughout the mature β‐layer, including the oberhautchen; 3) the concomitant presence of lipogenic lamellar bodies and PAS‐positive mucous granules in most presumptive α‐keratinizing cells; 4) the presence of the secreted contents of these organelles in the intercellular domains of the three derived tissues, the homologues of the squamate mesos, α‐, and lacunar cells; 5) the paucity of lamellated lipid deposits in such domains; 6) the presence of keratohyalin‐like granules (KHLG) in the presumptive lacunar, clear, and oberhautchen cells. In toto, the absence of many of the precisely definable, different pathways of cytogenesis discernible during squamate epidermal generation production might be interpreted as primitive for lepidosaurs. However, when the evolutionary significance of each of the six differences listed is evaluated separately, it becomes clear that the epidermis of S. punctatus possesses primitive amniote, shared and derived lepidosaurian, and some unique characters. This evaluation further elucidates the concept of a lepidosaurian epidermal generation as a derived manifestation of the sauropsid synapomorphy of vertical alternation of keratin synthesis and shows that further study of keratinocyte differentiation in the tuatara may contribute to our understanding of the origin and evolution of β‐keratinization in sauropsid amniotes. J. Morphol. 256:111–133, 2003. © 2003 Wiley‐Liss, Inc.
Dentition and tooth replacement pattern in Chalcides (Squamata; Scincidae)
Authors: Delgado Sidney , Davit‐Beal Tiphaine , Sire Jean‐Yves 
Published: March 2003

AbstractThis study was undertaken as a prerequisite to investigations on tooth differentiation in a squamate, the Canarian scincid Chalcides. Our main goal was to determine whether the pattern of tooth replacement, known to be regular in lizards, could be helpful to predict accurately any stage of tooth development. A growth series of 20 laboratory‐reared specimens, aged from 0.5 month after birth to about 6 years, was used. The dentition (functional and replacement teeth) was studied from radiographs of jaw quadrants. The number of tooth positions, the tooth number in relation to age and to seasons, and the size of the replacement teeth were recorded. In Chalcides, a single row of pleurodont functional teeth lies at the labial margin of the dentary, premaxillary, and maxillary. Whatever the age of the specimens, 16 tooth positions were recorded, on average, in each quadrant, suggesting that positions are maintained throughout life. Replacement teeth were numerous whatever the age and season, while the number of functional teeth was subject to variation. Symmetry of tooth development was evaluated by comparing teeth two by two from the opposite side in the four jaw quadrants of several specimens. Although the relative size of some replacement teeth fitted perfectly, the symmetry criterion was not reliable to predict the developmental stage of the opposite tooth, whether the pair of teeth compared was left–right or upper–lower. The best fit was found when comparing the size of successive replacement teeth from the front to the back of the jaw. Every replacement tooth that is 40–80% of its definitive size is followed, in the next position on the arcade, by a tooth that is, on average, 20% less developed. Considering teeth in alternate positions (even and odd series), each replacement tooth was a little more developed than the previous, more anterior, one (0.5–20% when the teeth are from 10–40% of their final size). The latter pattern showed that tooth replacement occurred in alternate positions from back to front, forming more or less regular rows (i.e., “Zahnreihen”). In Chalcides, the developmental stage of a replacement tooth in a position p can be accurately predicted provided the developmental stage of the replacement tooth in position p‐1 or, to a lesser degree, in position p‐2 is known. This finding will be particularly helpful when starting our structural and ultrastructural studies of tooth differentiation in this lizard. J. Morphol. 256:146–159, 2003. © 2003 Wiley‐Liss, Inc.
Variation in enterovirus receptor genes
Authors: Karttunen Åse , Pöyry Tuija , Vaarala Outi , Ilonen Jorma , Hovi Tapani , Roivainen Merja , Hyypiä Timo 
Published: March 2003

AbstractThe increased incidence of a enterovirus infections observed in patients with type 1 diabetes preceding the development of the clinical disease could be partially explained by variation in the genes coding for enterovirus receptors. We carried out sequence analysis of the most common enterovirus receptor molecules in 21 diabetic children and 20 healthy adults. DNA was isolated from the leukocytes, and gene regions known to code for virus‐recognizing domains in major enterovirus receptors were amplified and sequenced. Heterozygous single‐nucleotide polymorphism (SNP), Ala 67 (GCG) → Thr (ACG), was detected in the poliovirus receptor gene in four individuals in the diabetes group, but not in the control group. However, serological studies could not confirm that this substitution would convey different susceptibility to poliovirus infection. A heterozygous SNP, Lys 29 (AAG) → Met (ATG), was found in the intracellular adhesion molecule‐1 (ICAM‐1) (receptor for rhinoviruses and some coxsackie A viruses) in one individual in both groups. A silent SNP in the α2 integrin subunit gene (echovirus 1 receptor) was frequently found in both groups, a silent heterozygotic SNP in coxsackievirus‐adenovirus receptor (coxsackie B virus receptor) gene was seen in one individual in the diabetes group, whereas no variation was found in the DAF (echovirus receptor) and β3 integrin subunit sequences (receptor for coxsackievirus A9) studied. In conclusion, both synonymous and nonsynonymous sequence variability of genes coding for enterovirus and rhinovirus receptors was shown to occur, but no pattern directly specific for type 1 diabetes was found. J. Med. Virol. 70:99–108, 2003. © 2003 Wiley‐Liss, Inc.
Molecular and serological aspects of HBsAg‐negative hepatitis B virus infections in North America
Authors: Hsia C.C. , Scudamore C.H. , Di Bisceglie A.M. , Tabor E. 
Published: March 2003

AbstractA few hepatitis B virus (HBV) infections are characterized by the presence of HBV DNA in serum or liver tissue, or both, in the absence of detectable hepatitis B surface antigen (HBsAg) in serum. However, such infections have rarely been described previously in North American patients. In the present study, 31 hepatocellular carcinoma (HCC) patients from the United States and Canada who had no detectable HBsAg in their serum were studied. In these 31 HBsAg‐negative HCC patients, HBV DNA was detected in HCC and/or in adjacent nontumorous liver tissue using nested polymerase chain reaction (PCR) in 5/9 (56%) patients from the United States and in 12/22 (55%) from Canada. The 17 HBV DNA‐positive/HBsAg‐negative patients from the United States and Canada included 9 without any serological markers for HBV and 8 with detectable antibodies to hepatitis B core antigen. In these patients, HBV genotype C was the most prevalent genotype (11/17; 64%). HBV genotypes have not been previously reported in HCC patients from North America. Replicative intermediate forms of HBV (covalently closed circular HBV DNA) were detected in 2/17 (12%) HBV DNA‐positive/HBsAg‐negative patients, indicating that at least two of these patients had actively replicating HBV infections. The use of tests to detect HBV DNA permitted the identification of HBV infections in HBsAg‐negative HCC patients from North America. Among these patients, those with antibody to hepatitis C virus (HCV) would otherwise have been designated “HCV‐associated HCCs” based on serological tests alone. These findings provide a new perspective on determining the possible viral etiologies of HCCs in North America. J. Med. Virol. 70: 20–26, 2003. © 2003 Wiley‐Liss, Inc.
Prevalence of GBV‐C infection among dental personnel
Authors: Roy Kirsty M. , Bagg Jeremy , Kennedy Catherine , Cameron Sheila , Simmonds Peter , Lycett Carol , Hunter Iain , Taylor Margie 
Published: March 2003

AbstractHealthcare workers who carry out exposure‐prone procedures are theoretically at increased risk of acquiring blood‐borne virus infections. GB virus C (GBV‐C) is a recently described blood‐borne virus that is related distantly to hepatitis C virus. The occupational risk of GBV‐C infection to healthcare workers is unknown. This study collected detailed occupational and personal risk data in parallel with a blood specimen, to establish the prevalence and determinants of GBV‐C infection among dental healthcare workers. The presence of GBV‐C antibodies was detected using commercially available ELISA; GBV‐C RNA was detected by nested PCR using primers from the conserved 5′ noncoding region. The overall prevalence of GBV‐C antibodies among the study population was 11.1% (98/880, 95% confidence interval [CI], 9.1–13.4%) and 4.6% were positive for GBV‐C RNA (46/879, 95% CI, 2.5–5.1%), resulting in a cumulative prevalence of 15.7%. These figures are similar to those described in other populations. There was no significant difference in lifetime exposure to GBV‐C between dentists (17.7%) and dental nurses/hygienists (14.3%). Significantly more dental nurses/hygienists aged 16–30 years had been exposed to GBV‐C compared to dentists of the same age (χ2 = 13.75; P < 0.001). Conversely, significantly more dentists 46 years or older had evidence of exposure to GBV‐C compared to dental nurses/hygienists (χ2 = 6.79; P = 0.009). The high prevalence of GBV‐C infection did not seem to be related to past parenteral exposure, and the data suggest that sexual transmission, rather than occupational transmission, was a more important route for GBV‐C infection among this population. J. Med. Virol. 70:150–155, 2003. © 2003 Wiley‐Liss, Inc.
Identification of a unique BK virus variant in the CNS of a patient with AIDS
Authors: Jørgensen Gunn Eli Kimo , Hammarin Anna‐Lena , Bratt Gøran , Grandien Monica , Flægstad Trond , Johnsen John Inge 
Published: March 2003

AbstractHuman polyomavirus BK (BKV; GenBank or EMBL or DDBJ accession no. NC001538) is often reactivated in immunosuppressed patients. Reactivation has been associated primarily with excretion of the virus in the urine, and there have been few reports of renal and/or neurological disease caused by BKV in patients with acquired immunodeficiency syndrome (AIDS). Polymerase chain reaction, Southern blotting, and sequencing were used to detect and identify the noncoding control region (NCCR) of BKV in different tissues in an AIDS patient with meningoencephalitis, retinitis, and nephritis. An undescribed reorganized NCCR variant of the virus, completely different from the variants detected in peripheral blood leukocytes (PBLs) and urine, was identified in the cerebrospinal fluid (CSF) and CNS tissues. These results suggest that rearrangements in the NCCR of the virus have resulted in a BKV variant, which is better adapted to the host cell machinery of the cells in CNS tissue. The rearranged variant (BKV CNS) might have been involved in the initiation and/or development of the pathological lesions observed in the CNS‐related tissues of this patient. J. Med. Virol. 70: 14–19, 2003. © 2003 Wiley‐Liss, Inc.
Comparative evaluation of measles virus‐specific RT‐PCR methods through an international collaborative study
Authors: Afzal M.A. , Osterhaus A.D.M.E. , Cosby S.L. , Jin L. , Beeler J. , Takeuchi K. , Kawashima H. 
Published: March 2003

AbstractComparison of RT‐PCR assays established in house at various places revealed that laboratories could differ in sensitivity by as much as 1,000‐fold in terms of the ability to detect measles virus sequences in clinical samples. The study indicates that PCR findings, positive or negative, are questionable if they are not supported by the associated data demonstrating the overall sensitivity of the assay applied. Measles virus‐specific RT‐PCR‐based assays need to be validated using standard virus preparation or nucleic acid‐based target templates. A correlation between real‐time quantitative PCR and the conventional PCR for measles virus is highly desirable. J. Med. Virol. 70:171–176, 2003. © 2003 Wiley‐Liss, Inc.
Effect of the lipid peroxidation product acrolein on tau phosphorylation in neural cells
Authors: Gómez‐Ramos Alberto , Díaz‐Nido Javier , Smith Mark A. , Perry George , Avila Jesús 
Published: March 2003

AbstractA hallmark of several neurodegenerative disorders, including Alzheimer's disease and tauopathies, is the hyperphosphorylation of the microtubule‐associated protein tau. Tau phosphorylation by proline‐directed and non‐proline‐directed protein kinases has been tested using antibodies PHF1 and 12E8, respectively. The effect of the lipid peroxidation product acrolein on these modes of phosphorylation has been assayed. We have found that acrolein, a peroxidation product from arachidonic acid, increases the phosphorylation of tau at the site recognized by PHF‐1 both in human neuroblastoma cells and in primary cultures of mouse embryo cortical neurons. Whereas the basal phosphorylation of tau protein at the PHF1 site seems to be largely mediated by glycogen synthase kinase‐3 (which is also activated in response to Aβ peptide), the acrolein‐induced tau hyperphosphorylation at the same site is also due to p38 stress‐activated kinase. These results support the view that oxidative stress and subsequent formation of lipid peroxidation products may contribute to tau protein phosphorylation in Alzheimer's disease and tauopathies. © 2002 Wiley‐Liss, Inc.
High level of amyloid precursor protein expression in neurite‐promoting olfactory ensheathing glia (OEG) and OEG‐derived cell lines
Authors: Moreno‐Flores M. Teresa , Lim Filip , Martín‐Bermejo M. Jesús , Díaz‐Nido Javier , Ávila Jesús , Wandosell Francisco 
Published: March 2003

AbstractDuring all the life of a mammal, olfactory ensheathing glia (OEG) permit the entry and navigation of olfactory neuron axons from peripheral to central nervous system (CNS) territory. This physiological characteristic of OEG has been successfully used for promotion of axonal regeneration after CNS injury in animal models. However, cellular and molecular properties responsible for OEG regenerative ability remain to be unveiled. Two approaches may be followed: to carry out genomic or proteomic analysis to detect secreted and/or membrane bound molecules or to examine the expression of molecules previously described as neuritogenic. This is the case of amyloid precursor protein (APP), a neurite‐promoting molecule. We have studied the expression of APP by OEG and OEG‐derived clonal lines, immortalised with the large T antigen of SV40 (TEG lines). OEG express high levels of APP in vivo and in culture. TEG lines maintained high expression of APP. Western blot analysis showed the presence of high molecular weight forms of APP in OEG, corresponding probably to glycosylated forms and/or to higher expression of the full length APPs. The main APP isoforms present in OEG cultures were APP770 and 751. L‐APP isoforms without the exon 15, which are those corresponding with proteoglycan forms, are predominant in glial cells. Our data showed that OEG had three times as much L‐APP as astrocytes, which may correlate with OEG neuritogenic capacity. In conclusion APP, a neurite‐promoting molecule, is produced by OEG. Its nexin activity, dependent on the Kunitz family of serine protease inhibitors (KPI) domain and/or in combination with its glycosylation level might contribute with other factors to the ability of these cells to foster axonal elongation. © 2002 Wiley‐Liss, Inc.
Paracetamol effectively reduces prostaglandin E2 synthesis in brain macrophages by inhibiting enzymatic activity of cyclooxygenase but not phospholipase and prostaglandin E synthase
Authors: Greco Anita , Ajmone‐Cat Maria Antonietta , Nicolini Alessia , Sciulli Maria Gina , Minghetti Luisa 
Published: March 2003

AbstractEpidemiological studies indicate that nonsteroidal anti‐inflammatory drugs (NSAIDs) are neuroprotective, although the mechanisms underlying their beneficial effect remain largely unknown. Given their well‐known adverse effects, which of the NSAIDs is the best for neurodegenerative disease management remains a matter of debate. Paracetamol is a widely used analgesic/antipyretic drug with low peripheral adverse effects, possibly related to its weak activity as inhibitor of peripheral cyclooxygenase (COX), the main target of NSAIDs. As microglia play an important role in CNS inflammation and pathogenesis of neurodegenerative diseases, we investigate the effect of paracetamol on rat microglial cultures. Although less potent than other NSAIDs, (indomethacin ≃ NS‐398 > flurbiprofen ≃ piroxicam > paracetamol ≃ acetylsalicylic acid), paracetamol completely inhibited the synthesis of prostaglandin E2 (PGE2) in lipopolysaccharide‐stimulated microglia, when used at concentrations comparable to therapeutic doses. The drug did not affect the expression of the enzymes involved in PGE2 synthesis, i.e., COX‐1, COX‐2, and microsomal PGE synthase, or the release of the precursor arachidonic acid (AA). Paracetamol inhibited the conversion of exogenous AA, but not PGH2, into PGE2 indicating that the target of the drug is COX activity. Consistently, paracetamol inhibited with similar IC50 the synthesis of PGF2α and thromboxane B2, two other COX metabolites. Finally, none of the NSAIDs affected the productions of nitric oxide and tumor necrosis factorα, two inflammatory mediators released by activated microglia. As paracetamol was reported to inhibit PG synthesis in peripheral macrophages with an IC50 at least three orders of magnitude higher than in microglia, we suggest that this drug represents a good tool for treating brain inflammation without compromising peripheral PG synthesis. © 2003 Wiley‐Liss, Inc.
Variations in spare electron transport chain capacity: The answer to an old riddle?
Authors: Fern Robert 
Published: March 2003

AbstractSeveral neurological diseases involve focal injury of specific brain structures. Poisons of the electron transport chain complexes (ETCC) can also produce selective injury of brain structures when given systemically and have been implicated in the development of neurological disease. Why ETCC poisons damage particular brain regions is unclear. Calculations of the relative ETCC expression level to glucose utilization rate (GUR) ratio from published observations here reveal that a low ETCC/GUR ratio predisposes a brain structure to injury by a poison of that complex. While GUR can rise with increased neuronal activity, ETCC expression is fixed in the short term. A high ETCC/GUR therefore represents surplus ETCC capacity, allowing for increased ATP generation with short‐term increases in demand. A low ETCC/GUR indicates the opposite and will lead to energy failure when the specific ETCC is poisoned. These observations may explain why cyanide, a specific ETCC (IV) inhibitor, can produce selective injury of white matter, which has the lowest ETCC (IV)/GUR found in the brain. They are also consistent with the selective damage of the striatum produced by poisons such as rotenone, a form of injury implicated in Parkinson's disease. The striatum has a low ETCC (I)/GUR ratio, whereas rotenone is a selective ETCC (I) inhibitor. © 2003 Wiley‐Liss, Inc.
Modelling the southern extent of the last Icelandic ice‐sheet
Authors: Bingham Robert G. , Hulton Nicholas R. J. , Dugmore Andrew J. 
Published: March 2003

AbstractA three‐dimensional, time‐dependent numerical ice‐sheet model is used to investigate the southern extent of the last Icelandic ice‐sheet since the Last Glacial Maximum (LGM, ca. 20 000 14C yr BP). Ice development over southern Iceland is forced using a linear relationship between mass balance and altitude based on observations over Sólheimajökull, a southern outlet glacier of the Mýrdalsjökull ice‐cap. A continentality factor is introduced that raises inland equilibrium‐line altitudes (ELAs) and also slackens the mass‐balance/altitude gradient driving the model. With this calibration the present‐day ice distribution can be reconstructed. Growth from ice‐free to total ice cover is assessed and the sensitivity of ice extent to ELA change is shown to be non‐linear. The model indicates that an ELA lowering of 500 m, consistent with a ca. 5°C temperature depression for southern Iceland at the LGM, would enable glacier ice to cover the whole land surface within the modelled area and inundate any putative ecological refugia. Modelling with a 300 m ELA depression, consistent with previous reconstructions of Younger Dryas (YD, 10 000–11 000 14C yr BP) ice extent, indicates that the principal outcrops of the Sólheimar ignimbrite were glaciated at this time, suggesting that an origin during this stadial (and a correlation with North Atlantic Ash Zone I / Vedde Ash) is problematic. Copyright © 2003 John Wiley & Sons, Ltd.
Multiproxy Devensian Late‐glacial and Holocene environmental records at an Atlantic coastal site in Shetland
Authors: Whittington Graeme , Buckland Paul , Edwards Kevin. J. , Greenwood Malcolm , Hall Adrian M. , Robinson Marie 
Published: March 2003

AbstractMarine erosion at Clettnadal, West Burra island off the west coast of Shetland, caused the drainage of a small water body at Clettnadal, exposing deposits of Late Devensian and Holocene age. Pollen, diatom and invertebrate analyses have provided variable records of environmental change during stratigraphical event GI‐1. Event GS‐1 is revealed by the non‐pollen evidence, especially by Coleoptera, by sediment stratigraphy, and by radiocarbon dating. In contrast, the pollen evidence indicates that an arctic tundra flora, in which dwarf shrubs were prominent, persisted throughout the Late‐glacial. The Holocene brought colonisation by tree birch, but by ca. 9000 14C yr BP the taxon had almost disappeared. This contrasts strongly with other Holocene pollen records for Shetland where both Betula and Corylus avellana‐type survived longer—at some sites, for example, until ca. 2900 yr BP. The extreme westerly and exposed coastal situation of Clettnadal appears to be responsible both for a muted Late‐glacial response in the pollen record of terrestrial vegetation and for the early replacement of woodland by a maritime grassland. The results provoke questions concerning biological stability at times of marked climatic change. Copyright © 2003 John Wiley & Sons, Ltd.