bluuebunny/crossref_metadata_2025_split huggingface dataset:
Balanced chromosome abnormalities inv(16) and t(15;17) in therapy‐related myelodysplastic syndromes and acute leukemia: Report from an International Workshop†
Authors: Andersen Mette K. , Larson Richard A. , Mauritzson Nils , Schnittger Susanne , Jhanwar Suresh C. , Pedersen‐Bjergaard Jens 
Published: August 2002

AbstractThe Workshop identified 48 unselected patients with therapy‐related myelodysplastic syndrome or acute myeloid leukemia (t‐MDS/t‐AML) and inv(16), and 41 patients with t(15;17) after chemotherapy (CT) and/or radiotherapy (RT) for a malignant or nonmalignant disease. The primary diseases were: breast cancer, 33 patients; lymphomas, 24 patients; various other solid tumors, 30 patients; and nonmalignant diseases, 2 patients. The general type of previous therapy was RT only in 10 patients with an inv(16) and in 12 patients with a t(15;17), alkylating agents plus topoisomerase II inhibitors in 24 patients with an inv(16) and in 18 patients with a t(15;17), topoisomerase II inhibitors only in 5 patients with an inv(16) and in 2 patients with a t(15;17), alkylating agents only in 6 patients in each subgroup, and other types of chemotherapy in 3 patients in each subgroup. Most CT‐treated patients (69%) also received RT. The latency period to development of t‐MDS/t‐AML was short: a median of 22 months in patients with inv(16) and 29 months in patients with t(15;17). Twenty‐six patients (54%) with an inv(16) and 17 patients (41%) with a t(15;17) had additional cytogenetic abnormalities, which were unrelated to age and survival in both subgroups. Trisomy of chromosomes 8, 21, and 22 and del(7q) were the most frequent additional abnormalities in the inv(16) subgroup, whereas +8, −5, and del(16q) were most frequent in the t(15;17) subgroup. The disease was overt t‐AML in 38/48 patients (79%) with an inv(16) and in 38/41 patients (93%) with a t(15;17). Thirty‐three of 39 intensively treated patients (85%) with an inv(16) obtained a complete remission, whereas 24 of 35 intensively treated patients (69%) with a t(15;17) obtained a complete remission. The median overall survival of intensively treated patients was 29 months in both cytogenetic subgroups. In the inv(16) subgroup, patients younger than 55 years of age had a longer survival when compared with older patients (P = 0.006). The study supports the observation that t‐MDS/t‐AML with inv(16) and t(15;17) is often associated with prior therapy with topoisomerase II inhibitors; however, a notable finding was the high frequency of treatment with only radiotherapy, 29% of t(15;17) and 21% of inv(16). Response rates to intensive chemotherapy in this study were comparable to those of de novo disease. © 2002 Wiley‐Liss, Inc.
Prolonged survival of mouse epididymal spermatozoa stored at room temperature
Authors: Sato Masahiro , Ishikawa Aki , Nagashima Ayako , Watanabe Toshiteru , Tada Norihiro , Kimura Minoru 
Published: August 2002

AbstractSummary: The viability and fertility of isolated mouse epididymal spermatozoa kept for up to 7 days at various temperatures (4°C, 22°C, and 37°C) were determined. Spermatozoa kept for 3 days at 22°C were still active, while those kept at 37°C or 4°C exhibited great reduction in motility within 2 days after isolation. In vitro fertilizing abilities of spermatozoa left for 0, 1, 2, and 3 days at 22°C were 69.2, 32.5, 9.5, and 4.9%, respectively, when the cleavage rate to two‐cell stage was examined. Transfer of two‐cell embryos produced in vitro with spermatozoa left for 1, 2, and 3 days at 22°C resulted in production of fetuses with efficiencies of respectively 30.2, 11.5, and 16.7%, which were lower (63.3%) than that of embryos derived from in vitro fertilization with fresh spermatozoa. These findings indicate that spermatozoa kept for up to 3 days at 22°C can fertilize oocytes, although at relatively low efficiency. genesis 31:147–155, 2001. © 2001 Wiley‐Liss, Inc.
Myelin basic protein induces heme oxygenase‐1 in human astroglial cells
Authors: Businaro Rita , Fabrizi Cinzia , Caronti Brunella , Calderaro Caterina , Fumagalli Lorenzo , Lauro Giuliana M. 
Published: August 2002

AbstractHeme oxygenase‐1 (HO‐1), also known as heat‐shock protein 32 (HSP‐32), is induced in many cells by a large variety of stimuli. Its induction in nervous system cells following toxic and oxidative stress was suggested to play a protective role. Its presence was recently detected by immunohistochemical studies at the level of inflammatory lesions of rat experimental autoimmune encephalomyelitis. In the present study, we demonstrate that myelin basic protein (MBP) induces HO‐1 in human astroglial cells, as shown by Western blots and RT‐PCR. Proteolytic fragments derived from the whole MBP show a different behavior in the HO‐1 induction: MBP152‐167 was able to produce a light but still significant increase in HO‐1 mRNA and protein levels, whereas MBP68‐84 was not. The increase in HO‐1 production seems to be mediated by a Ca2+‐dependent mechanism, since MBP addition to astrocytoma cultures induced a strong and immediate increment of [Ca2+]i increase; MBP152‐167 elicited a delayed and less pronounced [Ca2+]i increase; no [Ca2+]i changes were induced following cell treatment with MBP68‐84. NO pathway involvement in the induction of HO‐1 by MBP was ruled out since the expression of the inducible isoform of nitric oxide synthase was not upregulated in treated cells, neither nitrite levels were modified, as demonstrated by Greiss reaction. The possible significance of HO‐1 induction following MBP stimulation is discussed. GLIA 37:83–88, 2002. © 2002 Wiley‐Liss, Inc.
Oligodendrocytes from human donors differ in resistance to herpes simplex virus 1 (HSV‐1)
Authors: Kastrukoff Lorne F. , Kim Seung U. 
Published: August 2002

AbstractPrimary cultures of human oligodendrocytes (HOLs) were established from six different donors. Differences in resistance to infection with herpes simplex virus 1 (HSV‐1) were determined between the primary cultures of HOL in tissue culture infective dose 50 (TCID50), indirect immunofluoresence (IF), and serial electron microscopy (EM) studies. Virus production at different multiplicities of infection (MOIs) indicated that differences in HSV‐1 replication were statistically significant and MOI‐dependent. Overall, virus yield from the HOL cultures infected at an MOI of 1 increased up to 6 days postinfection (PI); no additional enhancement occurred at 7 days PI. However, differences in the replication capacity of the six HOL cultures observed at 5 days PI persisted at 6 and 7 days PI. When taken together, the results of these investigations indicate that, similar to experimental animals, resistance to HSV‐1 differs between primary cultures of HOL and is donor‐dependent. The results also raise the possibility that similar to experimental animals, resistance to HSV‐1, mediated at the level of HOL, may be genetically determined. Furthermore, permissive infections of primary cultures of HOL were established with HSV‐1 over a wide range of MOIs, similar to results obtained with viral infection of primary murine oligodendrocytes, but neither latent nor abortive infections of HOL were induced in vitro, even at very low MOIs. Resistance to HSV‐1, mediated by glial cells, is a nonimmune mechanism that may influence the development of acute CNS infection in man as well as individual susceptibility to this virus. GLIA 38:87–92, 2002. © 2002 Wiley‐Liss, Inc.
Distribution of two splice variants of the glutamate transporter GLT‐1 in rat brain and pituitary
Authors: Reye Peter , Sullivan Robert , Scott Heather , Pow David V. 
Published: August 2002

AbstractWe have performed immunocytochemistry on rat brains using a highly specific antiserum directed against the originally described form of the glutamate transporter GLT‐1 (referred to hereafter as GLT‐1α), and another against a C‐terminal splice variant of this protein, GLT‐1B. Both forms of GLT‐1 were abundant in rat brain, especially in regions such as the hippocampus and cerebral cortex, and macroscopic examination of sections suggested that both forms were generally regionally coexistent. However, disparities were evident; GLT‐1α was present in the intermediate lobe of the pituitary gland, whereas GLT‐1B was absent. Similar marked disparities were also noted in the external capsule, where GLT1A labeling was abundant but GLT‐1B was only occasionally encountered. Conversely, GLT‐1B was more extensively distributed, relative to GLT‐1α, in areas such as the deep cerebellar nuclei. In most regions, such as the olfactory bulbs, both splice variants were present but differences were evident in their distribution. In cerebral cortex, patches were evident where GLT‐1B was absent, whereas no such patches were evident for GLT‐1α. At high resolution, other discrepancies were evident; double‐labeling of areas such as hippocampus indicated that the two splice variants may either be differentially expressed by closely apposed glial elements or that the two splice variants may be differentially targeted to distinct membrane domains of individual glial cells. GLIA 38:246–255, 2002. © 2002 Wiley‐Liss, Inc.
Transient expression of the NG2 proteoglycan by a subpopulation of activated macrophages in an excitotoxic hippocampal lesion
Authors: Bu Jie , Akhtar Nadia , Nishiyama Akiko 
Published: August 2002

AbstractCells that express the NG2 proteoglycan (NG2+ cells) constitute a large glial population in the normal mature rodent brain. They can differentiate into oligodendrocytes but are distinct from mature oligodendrocytes, astrocytes, microglia, and neurons. Changes in NG2+ cells were examined in kainic acid‐induced excitotoxic lesions of the hippocampus, and the relationship between NG2+ cells and reactive astrocytes and microglia was investigated between 1 and 90 days after lesioning. Two types of reactive NG2+ cells with altered morphology and increased NG2 immunoreactivity were observed in the lesion. Early changes, consisting of an increase in NG2 immunoreactivity and the number of processes, were apparent 24 h after lesioning and persisted through 3 months. These cells were distinct from reactive astrocytes or activated microglia/macrophages. A second type of reactive NG2+ cells appeared 2 weeks after injection, following an influx of macrophages. They had large, round cell bodies with short processes and expressed the microglia/macrophage antigens OX42 and ED1. Single cells coexpressing NG2 and macrophage/microglial antigens could be isolated from the lesion. The number of NG2+/OX42+ cells gradually declined and disappeared by 3 months after injection. They did not express glial fibrillary acidic protein or the alpha receptor for platelet‐derived growth factor, indicating that they are distinct from astrocytes or oligodendrocyte progenitor cells. Cells that coexpressed NG2 and OX42 were never observed in hippocampal slice cultures treated with kainic acid, suggesting that NG2+/OX42+ cells are not derived from endogenous resident brain cells. These findings demonstrate that NG2 expression is transiently upregulated on activated macrophages/microglia that appear during the chronic stage in an excitotoxic lesion in the adult CNS. GLIA 34:296–310, 2001. © 2001 Wiley‐Liss, Inc.
Apoptosis of inflammatory cells in immune control of the nervous system: Role of glia
Authors: Pender Michael P. , Rist Michael J. 
Published: August 2002

AbstractThe elimination of inflammatory cells within the central nervous system (CNS) by apoptosis plays an important role in protecting the CNS from immune‐mediated damage. T cells, B cells, macrophages, and microglia all undergo apoptosis in the CNS. The apoptotic elimination of CNS‐reactive T cells is particularly important, as these cells can recruit and activate other inflammatory cells. T‐cell apoptosis contributes to the resolution of CNS inflammation and clinical recovery from attacks of experimental autoimmune encephalomyelitis (EAE), an animal model of the demyelinating disease multiple sclerosis (MS). T‐cell apoptosis in the CNS in EAE occurs in both an antigen‐specific and an antigen‐nonspecific manner. In antigen‐specific T‐cell apoptosis, it is proposed that T cells that recognize their antigen in the CNS, such as CNS‐reactive T cells, are deleted by the process of activation‐induced apoptosis after activation of the T‐cell receptor. This may result from the ligation of T‐cell death receptors (such as CD95 (Fas) or tumor necrosis factor (TNF) receptor 1) by CD95 ligand (CD95L) or TNF expressed by the same T cell or possibly by microglia, astrocytes or neurons. Inadequate costimulation of the T cell by antigen‐presenting glial cells may render T cells susceptible to activation‐induced apoptosis. T cells expressing CD95 may also die in an antigen‐nonspecific manner after interacting with glial cells expressing CD95L. Other mechanisms for antigen‐nonspecific T‐cell apoptosis include the endogenous release of glucocorticosteroids, deprivation of interleukin‐2, and the release of nitric oxide by macrophages or glia. Apoptosis of autoreactive T cells in the CNS is likely to be important in preventing the development of autoimmune CNS diseases such as MS. GLIA 36:137–144, 2001. © 2001 Wiley‐Liss, Inc.
Peripheral astrocyte processes: Monitoring by selective immunostaining for the actin‐binding ERM proteins
Authors: Derouiche Amin , Frotscher Michael 
Published: August 2002

AbstractAstrocytes extend thin lamellate processes in the neuropil, in particular around synapses, where they can modulate synaptic function or mediate glial–neuronal communication. Previous studies have shown that these lamellate perisynaptic processes change their shape in response to neuronal activity, but the underlying mechanisms have remained unclear. Similarly, the molecular composition of these fine, sheet‐like astrocytic processes (often 50–100 nm wide) is not understood but has to be related to their dynamic properties. To this end, we have studied the presence of ezrin, radixin, and moesin (ERM proteins) in the rat hippocampus and in primary cultured astrocytes, applying immunoperoxidase, immunofluorescence, and immunogold techniques. These three ERM proteins are known as actin‐binding proteins that link the cell membrane to the actin cytoskeleton, particularly in microvillus‐bearing epithelial cells. In cell culture, anti‐ezrin and antiradixin, but not antimoesin, antibodies were specific for astrocytes, which often displayed selective staining of filopodia and microvilli. Nonoverlapping visualization of astrocytic peripheral and stem processes was obtained by immunocytochemical double labeling for ezrin and GFAP, respectively. In sections of rat hippocampus, homogeneous labeling of the neuropil, but not of cell layers, resulted from immunostaining of fine, peripheral astrocyte processes, as confirmed ultrastructurally. Our data show that the fine peripheral processes of astrocytes, which also constitute the perisynaptic glial sheath, are specialized in that they contain characteristic actin‐associated molecules, likely to contribute to their dynamic properties. Applying anti‐ezrin and anti‐radixin as selective markers, plasticity of these perisynaptic glial processes can be analyzed. GLIA 36:330–341, 2001. © 2001 Wiley‐Liss, Inc.
SCIP/Oct‐6, Krox‐20, and desert hedgehog mRNA expression during CNS remyelination by transplanted olfactory ensheathing cells
Authors: Smith P.M. , Sim F.J. , Barnett S.C. , Franklin Robin J.M. 
Published: August 2002

AbstractOlfactory ensheathing cells (OECs), although having a separate developmental origin to Schwann cells, are able to generate myelin sheaths following transplantation into areas of CNS demyelination that are remarkably similar to those made by Schwann cells. The transcriptional control of Schwann cell myelination has been well documented, in particular the role of SCIP/Oct‐6 and Krox‐20. It is not known, however, whether these transcription factors are also expressed when OECs assume a myelinating phenotype. In this study, we addressed this question by using a transplantation approach to generate myelinating OECs and then examined the expression of SCIP/Oct‐6 and Krox‐20 mRNA by in situ hybridization using oligonucleotide probes. We also examined the expression of desert hedgehog (Dhh), a Schwann cell–derived signaling molecule that is responsible for regulating the development of the connective tissue elements in peripheral nerve, which bear similarities to the morphologies adopted by nonmyelinating transplanted cells. Our results indicate that both Krox‐20 and Dhh mRNA are strongly expressed by transplanted OECs, with SCIP mRNA present at much lower levels. The expression of Krox‐20 relative to the expression of P0 mRNA by the transplanted OECs is consistent with its playing a similar role in OEC myelination to that in Schwann cell myelination, while the expression of Dhh suggests a possible mechanism for the diverse morphologies that cells adopt following OEC transplantation into the damaged CNS. Taken together, our results provide further evidence for the close similarity of OECs and Schwann cells and suggest that, despite their separate origins, the manner in which they generate a peripheral‐type myelin sheath involves similar regulatory mechanisms. GLIA 36:342–353, 2001. © 2001 Wiley‐Liss, Inc.
Three‐dimensional distribution of astrocytes in zebrafish spinal cord
Authors: Kawai Hitomi , Arata Noriko , Nakayasu Hiroshi 
Published: August 2002

AbstractWe prepared a monoclonal antibody (A‐22) that recognizes a 60‐kDa protein in the zebrafish brain. The antigen is distributed throughout the brain but is not found outside it. The antibody recognizes star‐shaped cells with long processes in the spinal cord. All A‐22‐positive cells are also GFAP‐immunopositive, but there are GFAP‐positive cells that are A‐22‐negative. The cells are connected to small veins and to the surface of the spinal cord. Immunopositive cells are generally homogeneous in size and shape and are found not only in the spinal cord but also in several areas of the brain. These results indicate that the stained cell is an astrocyte. Most of these cells (88%) are distributed in the gray matter of the spinal cord; the remainder (12%) are found in the white matter. Most of the cells in the gray matter are found in the ventral and dorsal horns, but some are also present in the central area along the ventricle. Glial cell bodies form an array along the longitudinal axis and are connected to each other by thick projections. The cellular array is not visible in coronal sections. In contrast, thin processes from the cells extend to the surfaces of veins, to neurons, and to the periphery of the spinal cord. We estimate that there are about 13,500 A‐22‐positive astrocytes in the spinal cord; however, this represents only 26% of the total number of astrocytes in the spinal cord (∼52,000). GLIA 36:406–413, 2001. © 2001 Wiley‐Liss, Inc.
Predictors of institutionalization of cognitively‐impaired elderly cared for by their relatives
Authors: Spruytte Nele , Van Audenhove Chantal , Lammertyn Frans 
Published: August 2002

AbstractObjectivesThe purpose of this study is to identify risk factors for nursing home placement of cognitively‐impaired elderly, with special attention to the role of psychosocial factors such as the caregiver's preference for institutionalization and the quality of the dyadic relationship.MethodsPartners, children and children‐in‐law caring for a relative suffering from dementia (n = 144) were interviewed at home. Sociodemographic variables, patient characteristics, characteristics of the caregiving situation, caregiver characteristics, the support with care and the quality of the caregiving relationship are included as predictors of the caregiver's preference for institutionalization and of the actual institutionalization six to nine months later. Data are analyzed using multiple (logistic) regression analyses.ResultsThe hypothesis that a poor quality of the relationship, besides other determinants, will be predictive of institutionalization received partial support. No relationship is found between the premorbid relationship quality and institutionalization (preference and actual). However, a good current relationship between the caregiver and the patient reduced the risk of nursing home placement. Institutionalization rate was 16.5% and it was predicted by the caregiver's preference for institutionalization, the functional level of the patient, the quality of the current relationship and the performance of accommodation changes at home.ConclusionResearch and interventions directed at delaying or preventing institutionalization should pay more attention to the role of psychosocial aspects in the process of nursing home placement. Specifically the relationship quality in terms of criticism or warmth might be a critical factor in the continuation of home care. Copyright © 2001 John Wiley & Sons, Ltd.
Sensory system interactions during simultaneous vestibular and visual stimulation in PET
Authors: Deutschländer Angela , Bense Sandra , Stephan Thomas , Schwaiger Markus , Brandt Thomas , Dieterich Marianne 
Published: August 2002

AbstractThe patterns of regional cerebral blood flow (rCBF) increases and decreases in PET were compared for unimodal vestibular, unimodal visual, and for simultaneous vestibular and visual stimulation. Thirteen healthy volunteers were exposed to a) caloric vestibular stimulation, b) small‐field visual motion stimulation in roll, c) simultaneous caloric vestibular and visual pattern stimulation. Unimodal vestibular stimulation led to activations of vestibular cortex areas, in particular the parieto‐insular vestibular cortex (PIVC), and concurrent deactivations of visual cortical areas [Brodmann area (BA) 17–19]. Unimodal visual motion stimulation led to activations of the striate visual cortex and the motion‐sensitive area in the middle temporal/middle occipital gyri (BA 19/37) with concurrent deactivations in the PIVC. Simultaneous bimodal stimulation resulted in activations of the cortical representation of both sensory modalities. In the latter condition activations and deactivations were significantly smaller compared to unimodal stimulation. The findings are consistent with the concept of an inhibitory reciprocal vestibulo‐visual interaction in all three stimulus conditions. Hum. Brain Mapping 16:92–103, 2002. © 2002 Wiley‐Liss, Inc.