bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tumor‐specific antigens in cutaneous T‐cell lymphoma: Expression and sero‐reactivity
Authors: Eichmüller Stefan , Usener Dirk , Thiel Daniela , Schadendorf Dirk 
Published: February 2003

AbstractCutaneous T‐cell lymphoma (CTCL) is a heterogeneous group of extra‐nodal non‐Hodgkin lymphomas with primary manifestation in the skin with poor treatment options in the advanced stages. As basis for future immune‐therapeutic strategies we have investigated the possible expression of tumor‐specific targets in CTCL focusing mainly on so‐called cancer‐germline genes. cDNAs derived from 20 CTCL tissues and 4 CTCL cell lines were tested with 15 gene‐specific and 4 gene family‐specific primers by RT‐PCR and confirmative Northern blotting. The most frequently detected mRNAs were LAGE‐1 (55% with only partial coexpression of the splicing variants), cTAGE‐1 (35%), MAGE‐A9 (27%) and the GAGE‐3–7 group (35%). Furthermore, we could detect NY‐ESO‐1 (21%) and a MAGE‐A subgroup (15%), whereas sub‐specification of the latter proved absence of MAGE‐A1, ‐A2, ‐A3, ‐A6 and ‐A12. SCP‐1 was found in only one specimen and a several antigens could not been detected in any tumor tissue or cell line (MAGE‐B, GAGE‐1,2,8 and all 4 RAGE genes). 90% of all CTCL samples were positive for at least 1 of the frequent mRNAs in RT‐PCR (LAGE‐1, NY‐ESO‐1, cTAGE‐1, MAGE‐A9, or GAGE‐3to7). Using a secondary SEREX approach we could detect sero‐reactivity in sera of CTCL patients against recombinant cTAGE‐1 (10/29), GAGE (3/19), MAGE‐A1 (1/18), ‐A3 (1/18), ‐A6 (2/18) and ‐A9 (4/18) protein, but not against LAGE‐1a, MAGE‐A4b or MAGE‐A12 protein (n = 19). We conclude, that certain cancer‐germline genes can be detected frequently in CTCL and are able to elicit a systemic immune response. These candidate genes might therefore be promising targets for immunotherapeutic interventions in CTCL. © 2003 Wiley‐Liss, Inc.
Macrophages in tumor‐draining lymph node with different characteristics induce T‐cell apoptosis in patients with advanced stage‐gastric cancer
Authors: Takahashi Akihiro , Kono Koji , Ichihara Fumiko , Sugai Hidemitsu , Amemiya Hideki , Iizuka Hidehiko , Fujii Hideki , Matsumoto Yoshiro 
Published: February 2003

AbstractA host's immune‐defense system is suppressive by many factors in patients with cancer. We have previously shown one possible mechanism behind the T‐cell dysfunction, whereby H2O2 secreted from macrophages in tumor‐draining lymph node (MTDL) induced T‐cell dysfunction with down‐regulation of TCR ζ molecules. In the present study, we analyzed how MTDL affect T cells, with a particular focus on T‐cell apoptosis, by co‐culturing MTDL with autologous peripheral blood T cells in gastric cancer. Moreover, we characterized the MTDL according to surface marker, oxygen‐burst capacity and intracellular cytokine status. T‐cell apoptosis was significantly induced in comparison to T‐cell alone control in patients with advanced disease, concomitant to the elevated caspase activity and following impaired T‐cell function. In patients with early disease, no significant difference was seen in the proportions of T cells that underwent apoptosis between T cells plus MTDL and T cells alone. Moreover, the addition of a selective scavenger of H2O2, catalase inhibited the apoptosis of T cells co‐cultured with MTDL in patients with advanced disease. In the characterization of MTDL, the production of H2O2 in MTDL from advanced disease was significantly higher than that in early disease. The amounts of intracellular IL‐10 and IL‐12 in MTDL in advanced disease were significantly higher than those in early disease. These results indicated that MTDL induced apoptosis of autologous T cells and this T‐cell dysfunction was mediated by H2O2 derived from MTDL. Furthermore, the characteristics of MTDL including the capacity of oxygen‐burst and intracellular cytokine production were different depending on the disease progression. © 2003 Wiley‐Liss, Inc.
Health profiles in 5836 long‐term cancer survivors
Authors: Schultz Pamela N. , Beck Martha L. , Stava Charles , Vassilopoulou‐Sellin Rena 
Published: February 2003

AbstractIncreasingly, prolonged survival follows the diagnosis of cancer. Cancer therapies result in complex and lasting health effects that create unique health‐care needs for the survivors but are poorly understood (especially in survivors of adult cancers). Cancer survivors were asked to respond to a mailed health survey and provide medical and social information pertaining to their cancer experience. Information about demographics and perceived disease‐related medical problems was analyzed. We analyzed the response of 5,836 survivors of adult cancers. Two‐thirds of the responses came from women, and the response rate was 51% in both sexes. The mean interval since cancer diagnosis was 18.0 ± 8.5 years. Younger survivors and men were more likely to report that cancer had affected their health. The health effect most commonly reported by survivors was arthritis/osteoporosis (26% of respondents). Survivors of Hodgkin's disease prominently reported thyroid and lung problems (33.8% of responders with the diagnosis). Prior diagnosis of lymphoma was associated with frequent mention of memory loss (14.7%). The passage of time decreased some perceived effects (memory loss) but increased others (arthritis/osteoporosis, cataracts). Compared with the general population, the incidence of several age‐ and gender‐adjusted health conditions in cancer survivors is different. This group of cancer survivors reported generally good health but outlined multiple lasting medical problems. The health survey described represents 1 approach to the development of comprehensive information about the health needs of cancer survivors. © 2003 Wiley‐Liss, Inc.
The molecular pharmacology of symplostatin 1: A new antimitotic dolastatin 10 analog
Authors: Mooberry Susan L. , Leal Rachel M. , Tinley Tina L. , Luesch Hendrik , Moore Richard E. , Corbett Thomas H. 
Published: February 2003

AbstractSymplostatin 1, an analog of dolastatin 10, was recently isolated from cyanobacteria of the genus Symploca. Symplostatin 1 is a potent inhibitor of cell proliferation with IC50 values in the low nanomolar range and it exhibits efficacy against a variety of cancer cell types. Symplostatin 1 caused the formation of abnormal mitotic spindles and accumulation of cells in metaphase at concentrations that had only minor effects on interphase microtubules. At higher concentrations, symplostatin 1 caused the loss of interphase microtubules. Cell cycle analysis revealed that symplostatin 1 caused G2/M arrest, consistent with its effects on mitotic spindles. Symplostatin 1 initiated the phosphorylation of Bcl‐2, formation of micronuclei and activation of caspase 3, indicating induction of apoptosis. The cellular effects of symplostatin 1 are consistent with other antimitotic tubulin‐targeting drugs. Tubulin polymerization experiments indicated that symplostatin 1 potently inhibits the assembly of purified tubulin, suggesting that tubulin may be its intracellular target. Some microtubule‐targeting agents are reported to have antiangiogenic activity and therefore the effects of symplostatin 1 on endothelial cell proliferation and invasion were evaluated. Symplostatin 1 was found to be a potent inhibitor of both endothelial cell proliferation and invasion. Because of its potent and broad activity in vitro, symplostatin 1 was evaluated in vivo. Symplostatin 1 was active against murine colon 38 and murine mammary 16/C; however, it was poorly tolerated and the mice were slow to recover from the toxicity. The data indicate that symplostatin 1 has a mechanism of action similar to dolastatin 10. © 2003 Wiley‐Liss, Inc.
Conditions ensuring starter induced 1‐factorizations are not isomorphic
Authors: Ihrig E. 
Published: February 2003

AbstractIn general, it is difficult to determine whether two starter induced 1‐factorizations of K2n are isomorphic. However, when one of the 1‐factorizations has a unique starter group to within conjugacy, we show that two starter induced 1‐factorizations on K2n are isomorphic, if and only if, the corresponding starters are isomorphic. Two starters are isomorphic if there is a group isomorphism between the respective starter groups which takes one starter to the other. It is relatively easy to check whether starters are isomorphic in many examples. The difficulty comes in showing there is a unique starter group to within conjugacy. A number of sufficient conditions for this are given; one such condition is the assumption that the 1‐factorization be irreducible, a condition which applies to all almost perfect 1‐factorizations. Also, generalized Mullin Nemeth starters are introduced and discussed in this context. © 2003 Wiley Periodicals, Inc. J Combin Designs 11: 124–143, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jcd.10023
Some results on the existence of large sets of t‐designs
Authors: Khosrovshahi G. B. , Tayfeh‐Rezaie R. 
Published: February 2003

AbstractA set of trivial necessary conditions for the existence of a large set of t‐designs, LS[N](t,k,ν), is $N\big | {{\nu \hskip -3.1 \nu}-i \choose k-i}$ for i = 0,…,t. There are two conjectures due to Hartman and Khosrovshahi which state that the trivial necessary conditions are sufficient in the cases N = 2 and 3, respectively. Ajoodani‐Namini has established the truth of Hartman's conjecture for t = 2. Apart from this celebrated result, we know the correctness of the conjectures for a few small values of k, when N = 2 and t ≤ 6, and also when N = 3 and t ≤ 4. In this article, we show that similar results can be obtained for infinitely many values of k. © 2003 Wiley Periodicals, Inc. J Combin Designs 11: 144–151, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jcd.10027
Lower bounds estimation of factor‐covering design sizes
Authors: Ido Nobuhiko , Kikuno Tohru 
Published: February 2003

AbstractFactor‐covering designs have been studied with the aim of making efficient suites of test cases for software testing. One of the major concerns in these studies is the construction of factor‐covering designs of smaller sizes. In this paper, we propose a method of estimating the lower bounds of the sizes. The proposed method is based on two assumptions that a test design has parameters of the same range, and that all the values in the range are tested equally. © 2003 Wiley Periodicals, Inc. J Combin Designs 11: 89–99, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jcd.10039
Intracellular fibroblast growth factor produces effects different from those of extracellular application on development of avian cochleovestibular ganglion cells in vitro
Authors: Bilak Masako M. , Hossain Waheeda A. , Morest D. Kent 
Published: February 2003

AbstractIn an avian coculture system, the neuronal precursors of the cochleovestibular ganglion typically migrated from the otocyst and differentiated in response to soluble fibroblast growth factor (FGF‐2), which had free access to FGF receptors on the cell surface. Free FGF‐2 switched cells from a proliferation mode to migration, accompanied by increases in process outgrowth, fasciculation, and polysialic acid expression. Microsphere‐bound FGF‐2 had some of the same effects, but in addition it increased proliferation and decreased fasciculation and polysialic acid. As shown by immunohistochemistry, FGF‐2 that was bound to latex microspheres depleted the FGF surface receptor protein, which localized with the microspheres in the cytoplasm and nucleus. For microsphere‐bound FGF‐2, the surface receptor‐mediated responses to FGF‐2 appear to be limited and the door opened to another venue of intracellular events or an intracrine mechanism. © 2003 Wiley‐Liss, Inc.
Oxidative neuronal death caused by glutamate uptake inhibition in cultured hippocampal neurons
Authors: Himi Toshiyuki , Ikeda Masayuki , Yasuhara Tadashi , Murota Sei‐itsu 
Published: February 2003

AbstractGlutamate transporters are coupled with cystine/glutamate antiporters to supply cystine as a component of glutathione, an important antioxidant. We sought evidence that L‐trans‐pyrrolidine‐2,4‐dicarboxylate (PDC) enhances glutamate‐induced neuronal damage not only via the N‐methyl‐D‐aspartate (NMDA) receptor mediated pathway, but also through induction of oxidative stress. Cultured hippocampal cells were exposed to glutamate (100 μM) for 5 min, washed and incubated for 18 hr with PDC (200 μM). PDC, increasing the neuronal death to 147% of that induced by glutamate alone, depleted glutathione in the culture, and produced dichloro‐dihydro‐fluorescein‐diacetate‐positive reactive oxygen species in neurons. N‐acetylcysteine (2 mM) not only reduced PDC‐enhanced neuronal death but also recovered glutathione and abolished the reactive oxygen species in these neurons. Threo‐β‐benzyloxyaspartate, another type of glutamate transporter inhibitor, also induced glutathione depletion in the glutamate‐preloaded cells, suggesting the involvement of glutamate transporter blocking in glutathione depletion. The NMDA receptor antagonist MK‐801, although partially effective in reducing PDC toxicity, slightly recovered glutathione level but did not reduce the reactive oxygen species even at a high concentration (100 μM). N‐acetylcysteine, dimethylsulfoxide, alpha‐phenyl‐N‐butyl nitrone and glutathione ethylester prevented neuronal death enhanced by PDC, but superoxide dismutase and catalase did not. Our study provides evidence that the block of glutamate uptake by PDC exerts toxicity on glutamate‐pretreated neurons not only through the accumulation of extracellular glutamate and subsequent activation of the NMDA receptor but also through depletion of glutathione and generation of reactive oxygen species. © 2002 Wiley‐Liss, Inc.
New component of the limbic system: Marginal division of the neostriatum that links the limbic system to the basal nucleus of Meynert
Authors: Shu Si Yun , Bao Xin Min , Ning Qun , Wu Yong Ming , Wang Jun , Leonard Brian E. 
Published: February 2003

AbstractThe limbic system refers to a group of connected neural regions that are associated with motivation, learning, and memory. The marginal division (MrD) is a zone located at the caudal border of the neostriatum in mammalian brains that has been shown to be involved in learning and memory. In a previous study, c‐fos expression showed functional connections between the MrD, basal nucleus of Meynert (NBM) and limbic system (Shu et al., 1988a, 1999). In the present study, to explore the relationship between these regions, the expression of limbic system‐associated membrane protein (LAMP) was investigated using molecular and immunohistochemical methods. Synaptic and functional connections between the MrD and the NBM were studied also using tract tracing, electron microscopic and behavioral methods. LAMP is thought to be a marker of the limbic system and expression of LAMP protein and mRNA was observed in both the MrD and the limbic system. From such results, it is concluded that the MrD is a new component of the limbic system. Fibers from the MrD were observed projecting and synapsing on cholinergic neurons of the NBM. As reduction of learning and memory was induced by lesioning the projection from the MrD to the NBM, it would seem that the MrD modulates the learning and memory function of the NBM. In conclusion, the results of these studies suggest that the MrD is a new component of the limbic system, and there are functional and structural connections between the MrD, NBM and limbic system. The MrD seems to act as a link between the limbic system and the NBM, and plays a role in learning and memory. © 2002 Wiley‐Liss, Inc.
Pyrrolidine dithiocarbamate‐induced neuronal cell death is mediated by Akt, casein kinase 2, c‐Jun N‐terminal kinase, and IκB kinase in embryonic hippocampal progenitor cells
Authors: Min Young Kyu , Park Jae Hyun , Chong Seon Ah , Kim Yun Sook , Ahn Young Soo , Seo Jeong Taeg , Bae Young Suk , Chung Kwang Chul 
Published: February 2003

AbstractPyrrolidine dithiocarbamate (PDTC) is known to induce cell death by the stimulation of intracellular zinc transport and subsequent modulation of nuclear factor‐κB (NF‐κB) activity. Zinc is a signaling messenger that is released by neuronal activity at many central excitatory synapses. Excessive synaptic release of zinc followed by entry into vulnerable neurons contributes to severe neuronal cell death. In the present study, we explored how PDTC modulates intracellular signal transduction pathways, leading to neuronal cell death. The exposure of immortalized embryonic hippocampal cells (H19‐7) to PDTC within the range of 1–100 μM caused cell death in a dose‐dependent manner. During the cell death, NF‐κB activity increased in response to PDTC, and this activity corresponded well with the increase of intracellular free zinc levels, implying that the activation of NF‐κB transmits the cell death signals of PDTC. Furthermore, PDTC caused the activation of IκB kinase (IKK), casein kinase 2 (CK2), phosphatidylinositol 3‐kinase (PI‐3K), and Akt, as well as mitogen‐activated protein kinases (MAPKs), such as extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK), but not p38 kinase. The blockade of PI‐3K, JNK, and CK2 pathways resulted in a remarkable suppression of PDTC‐induced cell death and also the activation of IKK, which subsequently led to a decrease of IκB phosphorylation. Although the overexpression of dominant‐negative SEK in a transient manner did not inhibit the activation of Akt by PDTC, the transfection of kinase‐inactive Akt mutants did cause a remarkable blockade of JNK activation, implying that Akt is present upstream of JNK in the PDTC‐signaling pathways. Moreover, whereas selective CK2 inhibitors suppressed PDTC‐induced JNK activation, the inhibition of JNK did not affect CK2 activity, suggesting that CK2 is directly related to the regulation of cell viability by PDTC and that the CK2‐JNK pathway could be a downstream target of PDTC. Taken together, our results suggest that PDTC‐mediated accumulation of intracellular zinc ions may affect cell viability by modulating several intracellular signaling pathways in neuronal hippocampal progenitor cells. © 2002 Wiley‐Liss, Inc.
Ein Sterilisationsprozess kann die Eigenschaften von Biokeramik verändern
Authors: Willmann G. 
Published: February 2003

AbstractBiokeramik auf Basis von bioinertem Aluminium‐ und Zirkonoxid, so wie bioaktivem Hydroxylapatit sind etablierte Werkstoffe für Implantate. Implantate müssen gereinigt und sterilisiert werden. Bei einigen Biokeramiken können beim Sterilisieren Veränderungen ihrer Farbe auftreten, die aber keinen ungünstigen Einfluß auf die Gebrauchseigenschaften haben. Das Sterilisieren mit Dampf im Autoklaven und mit Co60 Gamma Strahlung verursacht keinen Festigkeitsabfall bei Aluminiumoxidkeramik und bei dem neuen, keramischen Biokomposit AMC (Alumina Matrix Composite). Bei Y‐TZP Zirkonoxidkeramik dagegen wurde beim Sterilisieren mit Dampf ein Festigkeitsabfall gefunden.
Spinally generated electromyographic oscillations and spasms in a low‐thoracic complete paraplegic
Authors: Norton Jonathan A. , Wood Duncan E. , Marsden Jonathan F. , Day Brian L. 
Published: February 2003

AbstractWe have measured some oscillatory properties of severe lower limb spasms experienced by a low‐thoracic complete paraplegic during assisted standing. Electromyograms (EMG) were recorded from the leg muscles while the patient stood passively in a standing frame. The patient also stood using functional electrical stimulation (FES) while ground and handle reaction force vectors were measured together with EMG activity. During passive standing, spasms appeared simultaneously in all leg muscle groups on one side. The interval between spasms varied between 3 and 30 seconds. Within the spasms, there was a tendency of repetitive grouped discharge of motor units as well as a strong 10‐Hz component in the EMG that was coherent across ipsilateral muscle groups. Thus, the spasms were inherently oscillatory. During FES‐assisted standing, clinically similar spasms were observed. However, the interspasm interval became relatively fixed at around 16 seconds, which may indicate entraining of the spasm cycle by FES. There are similarities between this patient's spasms and the pathological motor activities seen in other movement disorders that may also be of spinal origin.
Secondary cervical dystonia associated with structural lesions of the central nervous system
Authors: LeDoux Mark S. , Brady Kimberly A. 
Published: February 2003

AbstractWe tested the hypothesis that structural lesions of the central nervous system (CNS) associated with cervical dystonia more commonly involve the cerebellum and its primary afferent pathways than basal ganglia structures. Cervical dystonia is the most common focal dystonia, the majority of cases are idiopathic, and only a small percentage of patients have a family history of dystonia or other movement disorders. Pathophysiological mechanisms operative in solely or predominantly appendicular dystonias such as writer's cramp and Oppenheim's dystonia, respectively, may not be directly applicable to axial dystonias. The localization of structural lesions of the CNS associated with secondary cervical dystonia may provide some insight into the neural structures potentially involved in primary cervical dystonia. The National Library of Medicine Gateway (from 1960) and a clinical database maintained by the senior author (from 1999) were searched for cases of secondary cervical dystonia associated with structural lesions of the CNS. Search terms included one or more of the following: dystonia, torticollis, cervical, secondary, and symptomatic. Lesion localization and type, patient age, patient gender, head position, occurrence of sensory tricks, and associated neurological findings were tabulated for each case. Structural lesions associated with cervical dystonia were most commonly localized to the brainstem and cerebellum. The remaining cases were equally divided between the cervical spinal cord and basal ganglia. Although inconsistent, head rotation tended to be contralateral to lesion localization. Additional neurological abnormalities were present in the majority of patients with secondary cervical dystonia. The relative paucity of basal ganglia pathology and concentration of lesions in the brainstem, cerebellum, and cervical spinal cord in patients with secondary cervical dystonia suggests that dysfunction of cerebellar afferent pathways may be important to the pathophysiology of primary cervical dystonia. © 2002 Movement Disorder Society
Pelvic movements as rhythmic motor manifestation associated with restless legs syndrome
Authors: Lombardi Carolina , Provini Federica , Vetrugno Roberto , Plazzi Giuseppe , Lugaresi Elio , Montagna Pasquale 
Published: February 2003

AbstractVideo‐polysomnographic monitoring of a patient with a 4‐year history of an unpleasant restless sensation originating in his lower abdomen showed stereotyped, repetitive, rhythmic pelvic body movements resembling coital behaviour at the wake–sleep transition. We discuss the association between restless legs syndrome and rhythmic movement disorder as a particular manifestation of a spectrum of rhythmic sleep‐related movement disorders.