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Transpl Int. 2003 Jun;16(6):367-75. Epub 2003 May 17.
Cardiac allograft vasculopathy: current concepts and treatment.

Waller J, Brook NR, Nicholson ML.

Division of Transplant Surgery, Professorial Unit, Leicester General Hospital, Leicester, Leicestershire, UK. juliaaller720.fsnet.co.uk

Cardiac allograft vasculopathy (CAV) remains the leading limiting factor of patient and graft survival after the first post-operative year. The pathogenesis involves both immunological and non-immunological factors. Here, we present recent advances and discuss potential preventative and treatment regimens. A review of the current literature of heart transplantation, detailing molecular mechanisms, pharmacological risk factors and novel immunosuppression regimens was performed. Recent findings demonstrate the pivotal role of the endothelium, resulting in release of pro-fibrotic cytokines, recruitment of circulating leucocytes, proliferation of vascular smooth muscle cells, and deposition of extracellular matrix proteins (ECMs). The role of HMG-CoA reductase inhibitors and anti-hypertensives remains controversial, but there is increasing evidence advocating their prophylactic use. We can conclude that novel immunosuppressive agents such as rapamycin, mycophenolate mofetil and FTY-720 are experimental immunosuppressive agents that are undergoing evaluation in clinical trials. The prophylactic use of statins and anti-hypertensive drugs needs to be defined but needs to suggest potential strategies to prolong cardiac allograft survival.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12756523&dopt=Abstract [PubMed - in process]

Mol Genet Genomics. 2003 May;269(2):243-51. Epub 2003 Mar 12.
Mapping of gene-specific markers on the genetic map of chickpea (Cicer arietinum L.).

Pfaff T, Kahl G.

Plant Molecular Biology, Biocenter, University of Frankfurt, Marie-Curie-Str. 9, Germany.

With the exception of the fact that it is made up of eight different chromosomes, the physical organization of the 738-Mb genome of the important legume crop chickpea (Cicer arietinum L.) is unknown. In an attempt to increase our knowledge of the basic structure of this genome, we determined the map positions of a series of genes involved in plant defence responses (DR) by genetic linkage analysis. Exploiting the sequence data available in GenBank, we selected genes known to be induced in chickpea and other plants by pathogen attack. Gene-specific primers were designed based on conserved regions, and used to detect the corresponding gene sequences in a segregating population derived from an interspecific cross between Cicer arietinum and C. reticulatum. Forty-seven gene-specific markers were integrated into an existing map based on STMS, AFLP, DAF and other anonymous markers. The potential of this approach is discussed.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12756536&dopt=Abstract

Mol Genet Genomics. 2003 May;269(2):271-9. Epub 2003 Mar 22.
Site-directed mutational analysis of the novel catalytic domains of alpha-aminoadipate reductase (Lys2p) from Candida albicans.

Guo S, Bhattacharjee JK.

Department of Microbiology, Miami University, Oxford, OH 45056, USA.

The alpha-aminoadipate reductase, a novel enzyme in the alpha-aminoadipic acid pathway for the biosynthesis of lysine in fungi, catalyzes the conversion of alpha-aminoadipic acid to alpha-aminoadipic-delta-semialdehyde in the presence of ATP, NADPH and MgCl(2). This reaction requires two distinct gene products, Lys2p and Lys5p. In the presence of CoA, Lys5p posttranslationally activates Lys2p for the alpha-aminoadipate reductase activity. Sequence alignments indicate the presence of all functional domains required for the activation, adenylation, dehydrogenation and alpha-aminoadipic acid binding in the Lys2p. In this report we present the results of site-directed mutational analysis of the conserved amino acid residues in the catalytic domains of Lys2p from the pathogenic yeast Candida albicans. Mutants were generated in the LYS2 sequence of pCaLYS2SEI by PCR mutagenesis and expressed in E. coli BL21 cells. Recombinant mutants and the wild-type Lys2p were analyzed for their alpha-aminoadipate reductase activity. Substitution of threonine 416, glycine 418, serine 419, and lysine 424 of the adenylation domain (TXGSXXXXK, residues 416-424) resulted in a significant reduction in alpha-aminoadipate reductase activity compared to the unmutagenized Lys2p control. Similarly replacement of glycine 978, threonine 980, glycine 981, phenylalanine 982, leucine 983 and glycine 984 of the NADPH binding domain (GXTGFLG, residues 978-984) caused a drastic decrease in alpha-aminoadipate reductase activity. Finally, substitution of histidine 460, aspartic acid 461, proline 462, isoleucine 463, glutamine 464, arginine 465, and aspartic acid 466 of the putative alpha-aminoadipic acid binding domain (HDPIQRD, residues 460-466) resulted in a highly reduced alpha-aminoadipate reductase activity. These results confirm the hypothesis that specific amino acid residues in highly conserved catalytic domains of Lys2p are essential for the alpha-aminoadipate reductase activity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12756539&dopt=Abstract

Parasitol Res. 2003 Jun;90(2):110-8. Epub 2003 Feb 11.
Structural and functional analysis of an amplification containing a PGPA gene in a glucantime-resistant Leishmania (Viannia) guyanensis cell line.

Anacleto C, Abdo MC, Ferreira AV, Murta SM, Romanha AJ, Fernandes AP, Moreira ES.

Departamento de Microbiologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, CP 486, CEP 31270-901, Belo Horizonte, MG, Brazil.

Drug resistance is a complex phenomenon in Leishmania and commonly involves gene amplification. Active efflux and metal sequestration through a P-glycoprotein have been pointed to as the major mechanisms used by drug-resistant Leishmania. A gene amplification from a glucantime-resistant Leishmania (Viannia) guyanensis cell line was characterised in an attempt to understand the mechanism of metal resistance in this pathogenic species. We show that the amplification is present as an extrachromosomal amplicon of 30 kb and contains a PGPA gene ( LgPGPA), which is overexpressed in the resistant line as shown by Northern and Western blot analyses. In addition, we gathered evidence from transfection experiments for the role of the LgPGPA gene in oxyanion resistance in L. (V.) guyanensis. Our work indicates that, in this pathogenic New World Leishmania species, amplification of the PGPA gene is the major determinant in oxyanion resistance.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12756544&dopt=Abstract

Pediatr Surg Int. 2003 Jul;19(5):380-4. Epub 2003 May 20.
Vascular changes play a role in the pathogenesis of necrotizing enterocolitis in asphyxiated newborn pigs.

Gellen B, Kovacs J, Nemeth L, Nemeth P, Vagvolgyi J, Bari F, Megyeri P, Pinter S, Temesvari P, Deli MA, Vecsernyes M, Szilvassy Z, Koltai M, Abraham CS.

Department of Paediatrics, University of Szeged, Koranyi fasor 14-15, 6720, Szeged, Hungary.

Necrotizing enterocolitis (NEC) is the most common acquired gastrointestinal emergency in neonates. We have developed an animal model of NEC in asphyxiated newborn pigs and investigated the effects of asphyxia on blood flow in superior mesenteric artery and abdominal aorta, cardiovascular data, arterial acid-base and blood gas parameters, and endothelial cytoskeletal structure in mesenteric microvasculature. Anesthetized, mechanically ventilated newborn pigs were included in two groups: piglets underwent severe asphyxia, and sham-operated control animals. A cardiovascular and metabolic failure developed in asphyxiated piglets approximately 1 h after the induction: severe hypotension and bradyarrhythmia were seen and significant reductions of the blood flow were measured in the superior mesenteric artery and abdominal aorta during the critical phase. Rearrangement of cytoskeletal actin structure corresponding to enhanced vascular permeability was seen with bodipy phallacidin in mesenterial endothelium of asphyxiated piglets after a 24-h recovery period. In conclusion, severe vasomotor changes during asphyxia may result in mesenteric endothelial dysfunction implicated in increased vascular permeability, edema formation, and development of NEC in asphyxiated piglets.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12756598&dopt=Abstract [PubMed - in process]

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