bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tumor necrosis factor receptor II (TNFRII) exon 6 polymorphism in systemic lupus erythematosus
Authors: Al‐Ansari A.S. , Ollier W.E.R. , Villarreal J. , Ordi J. , Teh L.‐S. , Hajeer A.H. 
Published: March 2003

Abstract:Systemic lupus erythematosus (SLE) is a complex autoimmune disease that exhibits extensive clinical heterogeneity. Several studies have suggested a role for tumor necrosis factor α (TNFα) in SLE and recently, the locus encompassing the TNF receptor II (TNFRII), which is a mediator of TNF effect, was amongst the candidate loci suggested by genetic linkage studies of multi‐case SLE families. Komata et al. reported an association between a polymorphism at position 196 (R allele) of TNFR II and SLE in Japanese patients. We have typed SLE patients from two different ethnic populations, Spanish and UK Caucasoids, for this polymorphism using a polymerase chain reaction and restriction fragment length polymorphism (PCR‐RFLP)‐based technique. No significant differences in allele or genotype frequencies were found between cases and matched controls in either population. The TNFRII 196R allele does not appear to be associated with SLE susceptibility in either Spanish or UK populations.
HLA‐A*2416: a new allele of the HLA‐A19 lineage
Authors: Binder T. , Heym J. , Horn B. , Blasczyk R. 
Published: March 2003

Acknowledgments:We would like to thank Cornelia Helfricht, Margit Saupe and Uta Schorner for expert technical assistance. This study was in part supported by a grant of the Wilhelm Sander‐Foundation.Abstract:We here report on a new HLA‐A19 allele (A*2416) found in a German kidney recipient. Serological class I typing revealed HLA‐A11,19 without clear definition of the A19 split antigen. As with serology, polymerase chain reaction (PCR)‐based typing also revealed inconclusive results. We therefore sequenced the gene from the 5′ flanking region through the 3′‐end of exon 4 of this allele after haplotype‐specific PCR amplification. The sequence analysis revealed a new HLA‐A allele which is identical to A*3101 with the exception of the 3′ half of exon 2 which is identical to the common A9 alleles. The phylogenetic analysis constructed with the nearest‐neighbor algorithm and based on exons 1–4 or introns 1–3 clearly indicated, that A*2416 belongs unequivocally to the A19 lineage ( Note).
Microsatellites in the HLA region: 1999 update
Authors: Foissac A , Salhi M. , Cambon‐Thomsen A. 
Published: March 2003

Abstract:In this third update of a series of reviews on microsatellites in the HLA region or close to it we report 155 microsatellites, corresponding to 51 newly described markers, in addition to the 103 reported in the 1997 and 1998 reviews. This work is based both on a literature review and on data publicly available in molecular databases on the internet ( http://www.gdb.org;
http://bioinfo.weizmann.ac.il/cards/;
http://cedar.genetics.soton.ac.uk/) up to September 1999. Thanks to numerous studies involving major histocompatibility complex (MHC) microsatellites, documentation on HLA region is proposed, including information on microsatellites described through MHC sequence projects and presenting documented location, polymorphism and amplification condition, together with additional information on previously described microsatellites when available and information on data in the literature regarding gametic associations between HLA region loci and alleles and microsatellite alleles. As basic information are presented various documents: i) a table showing the following characteristics of the 155 microsatellites: name, localisation, polymorphism, primer sequences, reference; ii) an integrated map of some HLA region genes and the 155 microsatellites considered; and iii) a summary table on HLA and microsatellites association patterns. In addition, an overview on HLA microsatellite analysis application is presented, with a special focus on disease genetics studies in the form of recent references where the use of microsatellites of the HLA region was a key tool. This review aims at providing the human immunogenetics community with a tool for helping optimal choice of microsatellites to be used in various studies.
Screening for the IDDM high‐risk genotype. A rapid microtitre plate method using serum as source of DNA
Authors: Cinek O. , Wilkinson E. , Paltiel L. , Saugstad O.D. , Magnus P. , Rønningen K.S. 
Published: March 2003

Abstract:Norwegian babies born with the HLA‐DRB1*0401‐DQA1*03‐DQB1*0302/DRB1*03‐DQA1*05‐DQB1*0201 genotype have an estimated 17% lifetime risk of developing insulin‐dependent diabetes mellitus (IDDM). Identifying these children is important for future prevention, and for studies of the non‐genetic factors involved in IDDM. The aim of the study was to develop a rapid screening method for this high‐risk genotype. DNA was extracted from serum collected during routine newborn screening for phenylketonuria and hypothyreosis. The second exons of HLA‐DQA1 and DQB1 were co‐amplified using biotinylated primers, amplicons were hybridized to a set of seven probes immobilized on a microtitre plate using a single hybridisation temperature, and detected colorimetrically by streptavidin‐HRP conjugate and tetramethylbenzidine substrate. The DRB1*04 subtyping was performed using six different probes at identical conditions. The prevalence of the DRB1*0401‐DQA1*03‐DQB1*0302/DRB1*03‐DQA1*05‐DQB1*0201 genotype among 1,026 Norwegian babies was 2.7% (CI 95%: 1.7–3.7%). The new high‐throughput genetic screening method for IDDM risk can easily be automated and included in newborn screening programs.
HLA‐B*1559: a hybrid allele including exon 2 of HLA‐B35 and exon 3 of HLA‐B15 and serologically typed as B35
Authors: Magira E. , Beznik‐Cizman B. , Monos D. 
Published: March 2003

Acknowledgments:This work was supported in part by office of Naval Research cooperative agreement # N‐00014‐96‐2‐0016 to the National Marrow Donor Program and by funding from the E.B. Foerderer Fund of the Children’s Hospital of Philadelphia to D.M.Abstract:The new allele HLA‐B*1559 described is of Hispanic origin. This allele carries the exon 2 of HLA‐B*35 alleles, and is identical to HLA‐B*3501 and the exon 3 of HLA‐B*1530. Serologically it is typed as B35. The most likely scenario for its generation seems to be a gene conversion event that involved the, frequent in Hispanic populations, B*1522 allele and a B*1530 allele. A segment of the B*1530 allele that included at least the sequences 412–419 would be transferred on a B*1522 background ( Note).
NEW ADVANCES IN THE MOLECULAR BIOLOGY OF ISCHEMIA/REPERFUSION: MAPK PATHWAYS
Authors: Toledo‐Pereyra LH , Lopez‐Neblina* F 
Published: March 2003

Ischemia/reperfusion (I/R) is an important pathological condition frequently associated with the organ/cell transplantation response. The molecular mechanisms involved in the development and characterization of the I/R lesion are represented, in some way, by the changes occurring in the intracytoplasmic phosphorylated proteins (MAPK) which transmit the I/R signal downstream to the nucleus. The MAPKinases are at the center of these developments. As an example, one of the MAPK signaling pathways is represented by the activation of NF‐kB. In this pathway, the MAPK phosphorilates the IkB fraction of the NF‐kB complex, allowing this fraction to be degraded by ubiquitination and proteolytic degradation by the ubiquitin‐proteome system. Free NF‐kB is translocated into the nucleus, with its subsequent effect on the activation and transcription of DNA with production of RNA, which would then copy the template of certain inflammatory cytokines (TNF‐α, IL1‐α, IL6), adhesion molecules (P‐selectin, E‐selectin, ICAM‐1, VCAM‐1) and chemokines (IL8) for future expression. At the same time, NF‐kB can be activated by TNF‐α and IL‐1, which would then reach TNFR1, TRADD, TRAF2, MEK, JNK and c‐Jun activation or return to the previous IkB route.MAPK pathways appear to be important in the regulation of the inflammatory response after I/R. p38, ERK and JNK are the best‐known MAPK systems, and their modification has direct implications for the I/R syndrome. Inhibition of p38 MAPK has been demonstrated to have a beneficial effect after various types of ischemia. ERK inhibition might play a role in the increased production of TNF‐α. The role of JNK is not as clear as the other two proteins. A better understanding of the MAPK regulatory mechanisms intervening in I/R would allow us to develop an improved and effective anti‐inflammatory therapy for this pathological condition.
JOINT PAIN AND ARTHRITIS IN RENAL TRANSPLANT RECIPIENTS, AND CORRELATION WITH CYCLOSPORINE THERAPY
Authors: Kart‐Köseoglu H , Yücel AE , Isýklar I , Türker I , Akçalý Z , Haberal M 
Published: March 2003

To determine the prevalence of joint pain and arthritis in renal transplant recipients, and to investigate relationships with various laboratory and clinical parameters.Eighty‐two patients who underwent renal transplantation (RT) and had a joint examination reported on their level of joint pain and arthritis by questionnaire. The patients were then followed for a year, with repeated joint examinations and laboratory tests every 3 months. Thirty‐one of 82 patients (37.8%) complained of joint pain before the RT, and seven of these 31 individuals reported continued pain after the operation. Seventeen of the 82 (20.7%) began to suffer joint pain after the RT. Six (7.3%) and three (3.7%) of the 82 patients developed arthritis before and after the transplantation, respectively. We found no statistical association between the joint pain and sex, age, cause of renal failure, dialysis duration, time since transplantation, bone mineral density, human leukocyte antigen type, serum levels of urate, parathormone, calcium, alkaline phosphatase, phosphorus, C‐reactive protein, erythrocyte sedimentation rate, donor source (living‐related or cadaveric), or presence of HCV infection. However, levels of serum cyclosporine higher than 200 ng/ml were significantly correlated with the joint pain. This study shows that joint pain is common before and after RT. In renal transplant recipients, joint pain is significantly correlated with serum cyclosporine levels.
RELATIONSHIPS BETWEEN HLA‐A, ‐B, ‐DQ AND ‐DR ANTIGENS AND INTERSTITIAL FIBROSIS IN RENAL ALLOGRAFTS
Authors: Özdemir BH , Çolak T , Turan M , Demirhan B , Haberal M 
Published: March 2003

Although renal transplant recipients tend to exhibit similar clinical and immunological changes over time, some allograft biopsies show early interstitial fibrosis (IF). To evaluate the relationship between HLA‐antigens and IF in renal allografts, we reviewed the HLA‐A, ‐B, ‐DQ, and ‐DR antigens in 88 renal transplant recipients.For each antigen type, we determined the number of patients who did and did not possess the antigen. We then determined the mean time to onset of IF for each of these two groups, and statistically compared the means. In the second part of the analysis, we divided the 88 patients into those who did and did not show IF at 6 months post‐transplantation, and then calculated the prevalence of each antigen type in the IF(+) and IF(–) groups. This same procedure was repeated with the patients grouped according to the presence of IF at 12 months post‐transplantation. The groups of patients with HLA‐B8, ‐B27, ‐DQ2, ‐DQ5, ‐DQ6, ‐DQ7, ‐DR4, ‐DR13, and ‐DR15, had significantly shorter times to IF onset after transplantation than the corresponding groups without these antigens (P<0.05). The groups that were IF(+) at 6 and 12 months post‐transplantation had significantly higher frequencies of HLA‐B8, ‐B27, ‐DQ2, and ‐DR4 than the corresponding IF(–) groups at these two timepoints (P<0.05).The results indicate that any kidney recipient with these antigens is predisposed to developing diffuse IF in their graft relatively soon after transplantation. We conclude that although there is multiple etiological agents in the pathogenesis of IF one can not exclude a HLA association in such cases.
RENAL TRANSPLANTATION OFFERS BETTER SURVIVAL IN HCV‐INFECTED END‐STAGE RENAL DISEASE PATIENTS
Authors: Siren S , Nurhan ÖF , Münire T , Sedat B , Zübeyde A , Mehmet H 
Published: March 2003

Hepatitis C virus (HCV) infection is known to increase morbidity and mortality in the dialysis population. Renal transplantation is an offered treatment option after a careful pretransplant evaluation. This study assessed the impact of HCV infection on patient and allograft survival rates in a selected group of dialysis patients and kidney transplant recipients.The study included 252 end‐stage renal disease patients who were receiving hemodialysis (HD) treatment or who received renal transplantation at our centre in 1995–96. Of the total, 116 [94 HCV (–) and 22 HCV (+)] underwent transplantation and 134 [106 HCV (–) and 30 HCV (+)] remained on HD. We retrospectively investigated 5 years of follow‐up findings in the records of these patients. All 22 HCV (+) individuals underwent liver biopsy to ensure there was no advanced liver disease before transplantation. None of the recipients or HD patients showed decompensation related to liver disease during follow up.The overall 5‐year patient survival rates for the kidney recipient and HD groups were 85.2% and 74.5%, respectively. Comparison of outcomes for the HCV (+) recipients had a significantly higher 5‐year survival rate than the HCV (+) HD patients (P<0.04). The 3‐year graft survival rates for the HCV (+) and HCV (–) transplant recipients were comparable, but the risks of chronic rejection and graft loss at 5 years were higher in the HCV (+) group (P<0.02, P<0.006, respectively). In conclusion, renal transplantation should be the preferred therapy in HCV‐infected dialysis patients because it improves the survival rates. HCV infection is associated with increased rates of chronic rejection and graft loss at 5 years post‐transplantation.
Practical protocols for stepwise solid‐phase synthesis of cysteine‐containing peptides
Authors: Angell Y. M. , Alsina J. , Barany G. , Albericio F. 
Published: March 2003

Abstract: This study details a series of conditions that may be applied to ensure ‘safe’ incorporation of cysteine with minimal racemization during automated or manual solid‐phase peptide synthesis. Earlier studies from our laboratories [Han et al. (1997) J. Org. Chem. 62, 4307–4312] showed that several common coupling methods, including those exploiting in situ activating agents such as N‐[(dimethylamino)‐1H‐1,2,3‐triazolo[4,5‐b]pyridin‐1‐ylmethylene]‐N‐methylmethanaminium hexafluorophosphate N‐oxide (HATU), N‐[1H‐benzotriazol‐1‐yl)‐(dimethylamino)methylene]‐N‐methylmethanaminium hexafluorophosphate N‐oxide (HBTU), and (benzotriazol‐1‐yl‐N‐oxy)tris(dimethylamino)phosphonium hexafluorophosphate (BOP) [all in the presence of N‐methylmorpholine (NMM) or N,N‐diisopropylethylamine (DIEA) as a tertiary amine base], give rise to unacceptable levels (i.e. 5–33%) of cysteine racemization. As demonstrated on the tripeptide model H‐Gly‐Cys‐Phe‐NH2, and on the nonapeptide dihydrooxytocin, the following methods are recommended: O‐pentafluorophenyl (O‐Pfp) ester in DMF; O‐Pfp ester/1‐hydroxybenzotriazole (HOBt) in DMF; N,N′‐diisopropylcarbodiimide (DIPCDI)/HOBt in DMF; HBTU/HOBt/2,4,6‐trimethylpyridine (TMP) in DMF (preactivation time 3.5–7.0 min in all of these cases); and HBTU/HOBt/TMP in CH2Cl2/DMF (1:1) with no preactivation. In fact, several of the aforementioned methods are now used routinely in our laboratory during the automated synthesis of analogs of the 58‐residue protein bovine pancreatic trypsin inhibitor (BPTI). In addition, several highly hindered bases such as 2,6‐dimethylpyridine (lutidine), 2,3,5,6‐tetramethylpyridine (TEMP), octahydroacridine (OHA), and 2,6‐di‐tert‐butyl‐4‐(dimethylamino)pyridine (DB[DMAP]) may be used in place of the usual DIEA or NMM to minimize cysteine racemization even with the in situ coupling protocols.
Transient vesicle leakage initiated by a synthetic apoptotic peptide derived from the death domain of neurotrophin receptor, p75NTR
Authors: Medina M.L. , Bolender J.P. , Plesniak L.A. , Chapman B.S. 
Published: March 2003

Abstract:  Peptides that induce apoptosis have potential as anticancer therapeutics. The design of safe, effective cancer therapeutic peptides requires characterization of the physical and chemical properties that influence activation of cell death in neoplastic cells. NTR365 is a synthetic pro‐apoptotic peptide with an amino acid sequence derived from the death domain of p75NTR. These studies were initiated to identify a potential mechanism for the apoptotic activity of NTR365 identified by Rabizadeh et al. We examined the interactions of this synthetic pro‐apoptotic peptide with phospholipid vesicles. Fluorescence experiments demonstrate that the peptide induces leakage from large unilamellar vesicles. Leakage activity is transient and dependent on the presence of anionic lipid in the vesicles. Circular dichroism studies show that the NTR365 adopts a different conformation and may have altered vesicle affinity under conditions conducive to leakage. The active conformation of NTR365 differs from that of the NMR derived conformation. A related peptide with a single substitution is not apoptotically active, does not form a helical structure in the presence of vesicles and does not induce appreciable vesicle leakage under the same conditions as NTR365. These studies suggest that the demonstrated apoptotic activity of a closely related NTR364 peptide is linked to disruption of a membrane barrier and to the ability of the peptide to form a helical structure.
Adventitious rooting in hypocotyls of sunflower (Helianthus annuus) seedlings. IV. The role of changes in endogenous free and conjugated indole‐3‐acetic acid
Authors: Liu Jin‐Hao , Reid David M. 
Published: March 2003

We have studied the role of endogenous auxin on adventitious rooting in hypocotyls of derooted sunflower (Helianthus annuus L. var. Dahlgren 131) seedlings. Endogenous free and conjugated indole‐3‐acetic acid (IAA) were measured in three segments of hypocotyls of equal length (apical, middle, basal) by using gas chromatography‐mass spectrometry with [13C6]‐IAA as an internal standard. At the time original roots were excised (0 h), the free IAA level in the hypocotyls showed an acropetally decreasing gradient, but conjugated IAA level increased acropetally; i.e. free to total IAA ratio was highest in the basal portion of hypocotyls. The basal portion is the region where most of root primordia were found. Some primordia were seen in this region within 24 h after the roots were excised. The quantity of free IAA in the middle portion of the hypocotyl increased up to 15 h after excision and then decreased. In this middle region there were fewer root primordia, and they could not be seen until 72 h. In the apical portion the amount of free IAA steadily increased and no root primordia were seen by 72 h.Surgical removal of various parts of the hypocotyl tissues caused adventitious root formation in the hypocotyl regions where basipetally transported IAA could accumulate. Reduction in the basipetal flow of auxin by N‐1‐naphthylphthalamic acid and 2,3,5‐tri‐iodobenzoic acid resulted in fewer adventitious roots. The fewest root primordia were seen if the major sources of endogenous auxin were removed by decapitation of the cotyledons and apical bud. Exogenous auxins promoted rooting and were able to completely overcome the inhibitory effect of 2,3,5‐tri‐iodobenzoic acid. Exogenous auxins were only partially able to overcome the inhibitory effect of decapitation. We conclude that in sunflower hypocotyls endogenously produced auxin is necessary for adventitious root formation. The higher concentrations of auxin in the basal portion may be partially responsible for that portion of the hypocotyl producing the greatest number of primordia. In addition to auxins, other factors such as wound ethylene and lowered cytokinin levels caused by excision of the original root system cuttings must also be important.
White light‐induced sugar distribution controls growth and osmotic properties in the coleoptile and the first leaf in Zea mays seedlings
Authors: Parvez Mohammad Masud , Wakabayashi Kazuyuki , Hoson Takayuki , Kamisaka Seiichiro 
Published: March 2003

The correlation of white light‐induced changes in osmotic concentration in the coleoptile and the first leaf and the growth rate of these organs in maize seedlings, was examined in relation to sugar distribution and invertase activity. One hour irradiation with white light decreased the osmotic concentration in basal zones of the coleoptile and increased it in the apical zones of the first leaf. The change in the osmotic concentration was positively correlated with the growth rate of both organs. The amount of total osmotic solutes in each zone was highly correlated with that of soluble sugars. Light decreased the activity of wall‐bound invertase in the coleoptile, but increased it in the first leaf. A high correlation existed between the content of soluble sugars and invertase activity in both organs. During 1 h incubation in the light, ca 2 µmol of soluble sugars per seedling was lost from the coleoptile and gained in the first leaf. Light promoted sugar exudation from the excised coleoptile, but the amount of soluble sugar exuded represented 5% of sugar loss from the coleoptile in intact seedlings.These results indicate that in maize seedlings white light controls the growth rate of the coleoptile and the first leaf through the osmotic concentration. Light may have an osmoregulatory function in the control of sugar distribution between the coleoptile and the first leaf by regulating the activity of wall‐bound invertase.
Genes with homologies to known α‐galactosidases are expressed during senescence of barley leaves
Authors: Chrost Bozena , Krupinska Karin 
Published: March 2003

α‐Galactosidase activity increases during dark induced senescence as well as during natural senescence under field conditions. Two cDNA clones named pHvSF11 and pHvSF23 were isolated from a cDNA library of senescent barley flag leaves by screening with a coffee bean α‐galactosidase cDNA as probe. Sequences of the two barley cDNAs show high homology to those of known α‐galactosidases and hence seem to represent two different α‐galactosidase genes in barley.Expression of the genes corresponding to HvSF11 and HvSF23 was analyzed on one hand in primary foliage leaves incubated in darkness to accelerate senescence and on the other hand in flag leaves from barley plants grown under field conditions. The transcript represented by the cDNA HvSF23 is detectable in fully expanded leaves and its level is slightly upregulated during dark induced senescence of primary foliage leaves as well as during natural senescence of flag leaves. In contrast, the level of the transcripts represented by the cDNA HvSF11 decreases in flag leaves during natural senescence and inversely increases in primary foliage leaves induced to senesce by darkness.Antibodies raised against overexpressed peptide sequences deduced from the two different partial cDNA sequences react with the same proteins. In extracts from primary foliage leaves induced to senesce by prolonged darkness two proteins were immunodecorated by these antibodies. In senescent flag leaves from a barley field an additional third protein was detected.