bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interleukin-7-Dependent Production of RANTES That Correlates with Human Immunodeficiency Virus Disease Progression
Authors: Llano Anuska , Barretina Jordi , Gutiérrez Arantxa , Clotet Bonaventura , Esté José A. 
Published: March 2003

ABSTRACT

There is a relationship between CD4-T-cell number and circulating interleukin 7 (IL-7) levels in human immunodeficiency virus (HIV)-positive individuals. Here, we show that IL-7 induced a dose-dependent production of CCL3 (MIP-1α), CCL4 (MIP-1β), and CCL5 (RANTES) in peripheral blood mononuclear cells (PBMC), ex vivo tonsil lymphoid tissue of HIV
−
individuals, and PBMC from HIV
+
individuals, suggesting that IL-7 may regulate β-chemokine production in vivo. In a cross-sectional study of HIV
+
individuals (
n
= 130), a weak but significant correlation between IL-7 and RANTES was noted (
r
= 0.379;
P
< 0.001). Remarkably, the correlation between IL-7 and RANTES increased to an
r
value of 0.798 (
P
< 0.001) if individuals with low CD4 cell counts (<200 cells/μl) were excluded from the analysis. Our results suggest that there is a relationship between IL-7 and the production of RANTES both in vitro and in vivo that is lost in immune-compromised patients (CD4 count of <200 cells/μl) but that could be restored by antiretroviral therapy. Unlike the case for IL-7, high levels of RANTES suggest an intermediate stage of HIV disease progression.
AN ALGORITHM FOR SCORE CALIBRATION BASED ON CUMULATIVE BAD RATES
Authors: SCHWALB OTTO , LEE TIMOTHY H. , ZHENG SHEN 
Published: March 2003

In credit scoring, it is sometimes desirable to implement a new score in place of an existing score. Let Y denote the existing score and let X denote the new score. It is almost always the case that the score ranges for X and Y are different. For example, the score range for X might be 0 to 100, while the score range for Y might be 300 to 600. It follows from this difference in score ranges that a major difficulty in implementing any new score will be in training those who use the existing score to use the new score. Score calibration is the process of constructing a calibration function g (·) in such a way that the calibrated score, g (X), is a score which mimics the behavior of Y. In applications, it is commonly found that problems in the distribution of g (X) arise as the result of the calibration process. There is a great need in production for an agorithm which automates the task of discovering these problems and correcting them. In this paper, we propose such a fully automatic algorithm. This algorithm has been successfully tested in many applications.
Defining and evaluating impact in environmental toxicology
Authors: Bailer A. John , Oris James T. , See Kyoungah , Hughes Michael R. , Schaefer Robert 
Published: March 2003

AbstractLegal mandates exist for the protection of wildlife and human health from the impacts of toxins released into the environment. To accomplish this objective, numeric environmental quality criteria are set. Toxicity test data are often analyzed in the development of such criteria. Regression‐based estimators are frequently employed to calculate the concentration associated with a specified decrement/inhibition in response relative to control conditions. Non‐monotonic concentration response patterns, often characterized as ‘hormesis’, may lead to alternative definitions of baseline responses for inhibition concentration calculations. In particular, the presence of hormesis may suggest that the definition of an impact measure is not always clear. In other cases, the impact measure may be clearly defined; however, adequate statistical study of such measures may not have been conducted. The bioconcentration factor, an index of how a toxicant accumulates within an aquatic organism relative to water, is an example where point estimates are often reported; however, reports of precision or confidence intervals are rare. A second example is the use of a no‐observed‐effect concentration, the highest concentration with responses that do not statistically differ from responses in the control group. Finally, multiple lines of evidence (e.g. toxicological, ecological, chemical, etc.) might be available to evaluate the degree of contamination at a particular site. The combination of this information to obtain overall site contamination assessment is a continuing challenge. These three issues provide a framework for discussing impact in environmental toxicology. Copyright © 2003 John Wiley & Sons, Ltd.
Suppression of EGFRvIII‐mediated proliferation and tumorigenesis of breast cancer cells by ribozyme
Authors: Luo Xunyi , Gong Xiaoqi , Tang Careen K. 
Published: March 2003

AbstractEGFRvIII is a tumor specific, ligand‐independent, constitutively active variant of the epidermal growth factor receptor. Its expression has been detected in many human malignancies including breast cancer. No detectable level of EGFRvIII has, however, been observed in adult tissues, including normal breast tissues. These unique features of the EGFRvIII make it an excellent target for biologically based therapies. We have designed and generated a tumor specific ribozyme targeted to EGFRvIII. This specific EGFRvIII ribozyme is able to effectively cleave EGFRvIII mRNA under physiological conditions in a cell‐free system, but does not cleave wild‐type EGFR and other EGF‐family receptors. While expressing this EGFRvIII‐ribozyme in breast cancer cells, EGFRvIII‐ribozyme is capable of downregulating endogenous EGFRvIII expression at the mRNA and protein levels. Inhibition of proliferation was observed in EGFRvIII‐ribozyme transfectants. In addition, downregulation of EGFRvIII in breast cancer cells significantly inhibited tumor growth in athymic nude mice. Furthermore, this ribozyme has no effect on EGF‐family receptor expression or the proliferation of breast cancer cells, which do not express EGFRvIII but express wild‐type EGFR and other EGF‐family receptors. These results suggest that we have generated a tumor‐specific, biologically functional ribozyme and further demonstrate that EGFRvIII plays a significant role in breast cancer cell proliferation. The ultimate goal of this approach is to provide a potential treatment for breast cancer by specifically targeting this receptor. © 2003 Wiley‐Liss, Inc.
A novel platinum compound inhibits telomerase activity in vitro and reduces telomere length in a human hepatoma cell line
Authors: Furuta Miho , Nozawa Katsura , Takemura Masaharu , Izuta Shunji , Murate Takashi , Tsuchiya Masayuki , Yoshida Kenji , Taka Naoki , Nimura Yuji , Yoshida Shonen 
Published: March 2003

AbstractTelomerase activity is detectable in most human tumors but not in most normal somatic cells or tissues. Telomerase inhibition has, therefore, been proposed as a novel and potentially selective strategy for antitumor therapy. In the present study, we found that platinum compounds, including cisplatin [cis‐diamminedichloro‐platinum (II)], strongly inhibited the activity of partially purified rat telomerase. Among the agents tested, 2,3‐dibromosuccinato [2‐(methylaminomethyl)pyridine]platinum (II) (compound E) exhibited the strongest inhibition, with an median inhibitory concentration (IC50) of 0.8 μM. The mode of inhibition was noncompetitive with either dNTPs or TS (first) primer, with Ki values estimated to be 2.3 or 3.9 μM for varied TS primer or dNTPs, respectively. Notably, cisplatin also inhibited the telomerase activity, with an IC50 of 2.0 μM. Again, the mode of inhibition was noncompetitive, with Ki values estimated as 7.3 or 8.1 μM. Preincubation of TS primer with compound E did not affect the telomerase inhibition, whereas preincubation with cisplatin caused remarkable enhancement. Treatment of a human hepatoma cell line HepG2 with a low concentration of compound E gradually reduced the telomere length, indicating that this compound was able to inhibit telomerase in living cells as well as in vitro. © 2003 Wiley‐Liss, Inc.
A new MICA allele with ten alanine residues in the exon 5 microsatellite
Authors: Pérez‐Rodríguez M. , Corell A. , Argüello J.R. , Cox S.T. , McWhinnie A. , Marsh S.G.E. , Madrigal J.A. 
Published: March 2003

Acknowledgments:This work is funded by the Anthony Nolan Bone Marrow Trust. We thank Dr. Gaby Fischer for technical support and critical reading of this manuscript.Abstract:The MICA and MICB genes code for protein products that have structural similarities to major histocompatibility complex (MHC) class I genes. These genes are upregulated by heat stress. They have been shown to interact with a common receptor (NKG2D/DAP10) on γδ T cells, CD8+ T cells and natural killer (NK) cells. The MICA gene has an expressed microsatellite, GCT, within the exon 5 which encodes for alanine. So far, four different repetitions of this short tandem have been reported. Also one non‐synonymous, one synonymous substitution and a 1‐bp insertion within this region have also been described. An association of Behçet’s disease with the microsatellite A9 has been reported. Here we report a novel allele with 10 GCT repetitions (A10) which was detected by reference strand mediated conformation analysis and confirmed by DNA sequencing.
Cloning and sequencing of canine MAGE cDNA
Authors: Ma Z. , Khatlani T.S. , Ohno K. , Sasaki K. , Inokuma H. , Onishi T. 
Published: March 2003

Abstract:Melanoma antigens (MAGE) are regarded to induce tumour‐specific immune response and thought to be potential therapeutical agents for cancer immunotherapy. We hereby report the canine MAGE cDNA cloned from the testis of a beagle dog. Canine MAGE cDNA is 1455 base pair (bp) nucleotides in length, and contains an open reading frame (ORF) of 1137 bp nucleotides encoding a protein of 378 amino acids. The predicted amino acid sequence has 22–49% of homology with other MAGE proteins. mRNA transcripts of canine MAGE were detected only in the melanoma and testis and not in other normal tissues of adult dog by reverse transcriptase‐polymerase chain reaction (RT‐PCR), indicating that the expression pattern of canine MAGE mRNA is similar to that of the MAGE family genes in tumor and normal tissues.
Identification of a new HLA‐B*39 allele: HLA‐B*3924
Authors: Cook J.T. , Day S. , Dunn P.P.J. , Welsh K.I. , Bunce M. 
Published: March 2003

Abstract:We have identified a new HLA‐B*39 allele through polymerase chain reaction (PCR) using sequence‐specific primers (SSP) and sequence‐based typing of exons 2 and 3. This novel allele was identified in three HLA‐identical siblings of Turkish origin. This allele only differs from HLA‐B*3903 at a unique single nucleotide substitution (T for C) at position 365 in exon 3 which results in an amino acid change in codon 98 of methionine (ATG) to threonine (ACG). The sequencing enabled the development of a monospecific PCR‐SSP reaction which can be used to discriminate between HLA‐B*3924 and other B*39 alleles.
Incomplete penetrance of MHC susceptibility genes: prospective analysis of polygenic MHC‐determined traits
Authors: Alper C.A. , Awdeh Z. 
Published: March 2003

Abstract:We propose an approach to understanding incomplete penetrance of disease susceptibility genes as a method of studying the underlying mechanisms of polygenic diseases. Incomplete penetrance is the failure of genetically susceptible individuals to exhibit a trait. We define as baseline penetrance that which occurs in genetically identical (monozygotic) twins of an index subject with a major histocompatibility complex (MHC)‐associated disease or trait. We consider two mechanisms for incomplete baseline penetrance: an extrinsic (environmental) trigger and an intrinsic stochastic, gene‐associated process. The latter can be detected for dominant expression because susceptibility genes in homozygotes (with their two intrinsic triggers) will be up to twice as frequently penetrant as those in heterozygotes. The extent of MHC and non‐MHC gene contribution determines differences between baseline penetrance and apparent penetrance in MHC‐identical sib pairs, sib pairs in general and MHC‐identical unrelated individuals. Inheritance patterns in families do not reveal modes of inheritance of incompletely penetrant polygenic MHC‐determined traits. A method is proposed to study such traits prospectively in persons presumed to be homozygous, heterozygous or non‐carrying for susceptibility genes by determining trait expression in homozygotes, heterozygotes or non‐carriers of trait‐associated conserved extended MHC haplotypes. The method provides direct estimates of apparent penetrance rates, modes of genetic determination, and, if the trait is dominant, the origin of penetrance. When applied to dominant MHC susceptibility gene‐determined immunoglobulin deficiencies in two populations, the ratios of affected haplotype homozygotes to heterozygotes near 2.0 were consistent with an intrinsic mechanism for baseline penetrance acting on the MHC susceptibility genes.
Wide distribution of the MICA‐MICB null haplotype in East Asians
Authors: Komatsu‐Wakui M. , Tokunaga K. , Ishikawa Y. , Leelayuwat C. , Kashiwase K. , Tanaka H. , Moriyama S. , Nakajima F. , Park M.H. , Jia G.J. , Chimge N.‐O. , Sideltseva E.W. , Juji T. 
Published: March 2003

Abstract:Stress‐inducible MICA (MHC class I chain‐related A) is known to bind to NKG2D, which is one of the natural killer (NK) cell receptors, and plays a role in immune surveillance. We have reported that a MICA‐MICB null haplotype is in linkage disequilibrium with HLA‐B*4801 in the Japanese population. In the haplotype, an approximately 100‐kb deletion, including the entire MICA gene, was observed and MICB possessed a premature stop codon. In this study, a multiplex polymerase chain reaction (PCR) method was developed for detecting the MICA deletion. MICB alleles were typed by PCR‐single‐strand conformation polymorphism (SSCP) method and direct sequencing. The frequency of the MICA‐MICB null haplotype was 3.7% on the average, and was strongly associated with HLA‐B48 in seven East Asian populations. It was presumed that the stop codon of MICB gene generated after the large‐scale deletion. The wide distribution of the null haplotype at polymorphic frequencies suggests that the haplotype has been conservatively maintained because of some selective advantage.
Identification of HLA‐A*2306
Authors: Cox S.T. , McWhinnie A.J. , Baker F.A. , Stubbins M.J. , Allen C.J. , Holman R. , Madrigal J.A. , Little A.‐M. 
Published: March 2003

Abstract:We describe a novel allele encoding HLA‐A23: A*2306, discovered in an African‐American individual, whose DNA was HLA typed as part of a quality control exercise. Direct sequencing typing identified A*2301 and A*6601 with an unexpected heterozygous peak at position 331. As position 331 is at the end of exon 2, near the priming site for the B3.6 anti‐sense sequencing primer, the sequencing data is not optimal in this region and sequencing from the sense primer is relied on. In addition the new polymorphism was not at an expected polymorphic position and could easily have been missed, leading to the assignment of A*2301. However, data from reference strand mediated conformation analysis showed distinct new mobilities from those expected for A*2301 with two different fluorescent‐labelled references, leading to the conclusion that the heterozygous peak seen at position 331 was a true variant of the A*2301 allele. A*2306 is most similar to A*2301 with 1 nucleotide difference at position 331 in exon 2 which was previously a conserved position. This mutation results in an amino acid substitution of glutamine for glutamate at residue 87 (Note).
Identification of a novel DRB1 allele, DRB1*1112, by sequence‐based DRB typing
Authors: Luo M. , Blanchard J. , Maclean I. , Brunham R. 
Published: March 2003

Abstract:We report here a novel DRB1 allele (DRB1*1112) identified during sequence‐based HLA‐DRB typing. Polymerase chain reaction with generic DRB primers and group‐specific primers and subsequent sequencing yielded identical results. Molecular cloning and sequencing confirmed that the new DRB1 allele is identical to DRB1*11011 and 1129 at exon 2 except for a single nucleotide substitution at codon 37, changing the codon from Tyr (DRB1*11011) or Ser (DRB1*1129) to Phe (Note).
EFFECTS OF HLA MISMATCHING ON GRAFT SURVIVAL IN LIVING DONOR‐KIDNEY TRANSPLANTATION
Authors: Haberal M , Emiroğlu R , Başaran Ö , Tezel E , Karakayalý H , Bilgin N 
Published: March 2003

To investigate the influence of HLA match on graft survival, we evaluated 878 live‐donor and 183 cadaver‐donor kidney transplantations performed at our hospital between October 1985 and November 2001. In the 878 live‐donor cases, 273 of the donors were mothers, 131 were fathers, 281 were siblings, 28 were offspring, 89 were second‐degree relatives, and 76 were unrelated (68 spouses and eight emotionally attached friends).The 1‐, 3‐, and 5‐year graft survival rates in the first‐degree living‐related transplantation group were 90%, 76%, and 66%, respectively. The corresponding rates in the second‐degree living‐related group were 90%, 75%, and 70%, respectively; and in the living‐unrelated group were 80%, 70%, and 60%, respectively. The 1‐, 3‐, and 5‐ year graft survival rates for the cadaveric kidney transplantations carried out at our center during this same time period were 78%, 60%, and 48%, respectively. These rates were significantly lower than those for each of the live‐donor transplantations. We analyzed graft survival in relation to HLA mismatch, and a comparison of the findings showed that 0‐mismatched cases had a statistically significant graft survival advantage over those with 1, 2, 3,4 and 5 mismatches; however, there were no significant differences between the groups with 1, 2, 3, 4 and 5 mismatches. In conclusion, even kidneys from live donors in transplantations with suboptimal donor‐recipient HLA matching show better 5‐year survival than cadaveric grafts in transplantations. These results from a single centre suggest that immunological as well as nonimmunological factors are associated with the pathogenesis of late graft loss.
EFFECT OF GRAFT NEPHRECTOMY AND HLA TYPING ON LONG‐TERM GRAFT FUNCTION AND SURVIVAL IN KIDNEY RETRANSPLANTATION
Authors: Karakayalý H , Yağmurdur MC , Moray G , Tezel E , Emiroğlu R , Haberal M 
Published: March 2003

In this study, we retrospectively evaluated our long‐term results of the recipients who received a second allograft. Between 3 November 1975 and 31 December 2001, our transplantation team performed 1365 kidney transplantations. Fifty (3.6%) of these patients underwent retransplantations. Forty‐seven received their second transplantation and the remaining three received their third transplantation. The same low‐dose triple drug immunosuppression protocol with prednisolone, azathioprine and cyclosporine A was used in both groups. There were two study groups: the patients in Group 1 (n=19) underwent allograft nephrectomy, while those in Group 2 (n=31) did not. Demographic properties, rejection rates throughout the follow up period, serum creatinine levels within 12 months, graft and patient survival rates, postoperative complications, time interval between the transplantations, and HLA matchings were studied. For statistical analysis the Student's t and Kaplan–Meier tests were used, and P‐values <0.05 were accepted as significant.Forty‐one patients who underwent re‐transplantation received kidney from living related donors and remaining 9 patients from cadaveric donors. Mean interval between first and second transplantations was 50 months (range, 1–192 months). Mean blood creatinine levels was 1.8 mg/dL (range, 0.8–6.5 mg/dL). HLA‐AB and HLA‐DR mismatches were 1.92±1.1 and 0.9±0.7, respectively.Acute rejection rates were significantly different between Group 1(9/19,47%) and Group 2(12/31,38%) (P=0.03). Graft loss was found to be lower in Group 1 (6/19, 32%) than that in Group 2 (11/31 35%), though these values were not statistically different (P>0.05). The average interval between first and second transplantations was 32,1±21 months in Group 2 and 61,5±46 months in Group 1 (P=0.018). The duration of hemodialysis before second transplantation were 17±9 months in Group 2 and 27±11 months in Group 1 (P=0.04). One, 3 and 5 years graft survival rates (Group 2 vs. Group 1) were 89% vs. 83%, 79% vs. 64% and 68% vs. 45%, respectively (P<0.05). Also, the interval between first and second transplantations may have a negative correlation with second graft survival In conclusion, there appears to be no advantage associated with graft nephrectomy before re‐transplantations and longer duration of hemodialysis may decrease graft survival rates.
Binding of agonists, antagonists and inverse agonists to the human δ‐opioid receptor produces distinctly different conformational states distinguishable by plasmon‐waveguide resonance spectroscopy
Authors: Salamon Z. , Hruby V. J. , Tollin G. , Cowell S. 
Published: March 2003

Abstract: Structural changes induced by the binding of agonists, antagonists and inverse agonists to the cloned δ‐opioid receptor from human brain immobilized in a solid‐supported lipid bilayer were monitored using plasmon‐waveguide resonance (PWR) spectroscopy. Agonist (e.g. deltorphin II) binding causes an increase in membrane thickness because of receptor elongation, a mass density increase due to an influx of lipid molecules into the bilayer, and an increase in refractive index anisotropy due to transmembrane helix and fatty acyl chain ordering. In contrast, antagonist (e.g. TIPPpsi) binding produces no measurable change in either membrane thickness or mass density, and a significantly larger increase in refractive index anisotropy, the latter thought to be due to a greater extent of helix and acyl chain ordering within the membrane interior. These results are closely similar to those reported earlier for another agonist (DPDPE) and antagonist (naltrindol) [Salamon et al. (2000) Biophys. J.79, 2463–2474]. In addition, we now find that an inverse agonist (TMT‐Tic) produces membrane thickness, mass density and refractive index anisotropy increases which are similar to, but considerably smaller than, those generated by agonists. Thus, a third conformational state is produced by this ligand, different from those formed by agonists and antagonists. These results shed new light on the mechanisms of ligand‐induced G‐protein‐coupled receptor functioning. The potential utilization of this new biophysical method to examine structural changes both parallel and perpendicular to the membrane normal for GPCRs is emphasized.
Responses of the transcriptional apparatus of barley chloroplasts to a prolonged dark period and to subsequent reillumination
Authors: Krause Kirsten , Falk Jon , Humbeck Klaus , Krupinska Karin 
Published: March 2003

In this study the responses of the chloroplast transcriptional apparatus in barley (Hordeum vulgare L. cv. Carina) primary foliage leaves were examined during and after interruption of the light/dark growth regime by a two‐day period of light deprivation on days 10 and 11 after sowing.Run‐on transcript assays and northern blot analyses showed that transcripts in chloroplasts can be divided into at least three groups that differ in their levels during the dark period and in the kinetics of their resynthesis during the reillumination phase. Group I transcripts (rbcL, psaA,B, atpB) show decreased expression as well as reduced transcript accumulation during the dark period both of which are restored within 32 h after reillumination of the plants. Group II (psbA, psbD) and group III (16S rRNA, trnE) transcripts show a delayed or no detectable response to prolonged darkness at the transcript level. While group II transcription does not change significantly upon reillumination, transcription of group III genes increases substantially above the initial value within a very short time after retransfer into light.Changes in gene specificity of the transcriptional apparatus are accompanied by a changing sensitivity of the chloroplast transcriptional apparatus towards the transcription inhibitor tagetitoxin. The strongest inhibitory effect of tagetitoxin could be observed in leaves recovering from the dark‐induced stress situation.