Influence of delayed graft function in renal transplants from cadaveric or non-heart-beating donors.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Jain.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The current treatment of posttransplant lymphoproliferative disease (PTLD) includes prophylaxis at the time of transplant, decreasing or stopping immunosuppresion and initiation of antiviral therapy in patients with polymerase chain reaction or clinical evidence of PTLD, and judicial reintroduction of immunosuppression in patients who have cleared their PTLD and have begun to have rejection. The pharmacology, pharmacokinetics, notable side effects, and toxicities of the immunosuppressive agents are described in this article. At the conclusion of each section the author's current practice with these agents and treatment strategies are described.
OBJECTIVES: Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by expansion of GAA repeats in the frataxin gene. We have carried out the first molecular analysis at the Friedreich's ataxia locus in the Indian population. MATERIALS AND METHODS: Three families clinically diagnosed for Friedreich's ataxia were analyzed for GAA expansion at the FRDA locus. The distribution of GAA repeats was also estimated in normal individuals of Indian origin. RESULTS: All patients clinically diagnosed for Friedreich's ataxia were found to be homozygous for GAA repeat expansion. The GAA repeat in the normal population show a bimodal distribution with 94% of alleles ranging from 7-16 repeats. CONCLUSION: Indian patients with expansion at the FRDA locus showed typical clinical features of Friedreich's ataxia. The low frequency of large normal alleles (6%) could indicate that the prevalence of this disease in the Indian population is likely to be low.
Explore the source record for details and available documents.
BACKGROUND: Renal ischaemia-reperfusion (IR) injury is an inevitable consequence of transplantation and contributes to later graft fibrosis. This study aimed to elucidate the possible mechanisms by studying the expression of genes associated with extracellular matrix (ECM) turnover. METHODS: Male Wistar rats underwent laparotomy, clamping of the right renal pedicle for 45 min, and left nephrectomy. Control animals underwent left nephrectomy only, or had no operation. Animals were killed at 8, 16 and 24 weeks and messenger RNA was extracted from renal tissue. Genes of interest were amplified and then quantified in an enzyme-linked immunosorbent assay system with levels expressed as a ratio to a known housekeeping gene (GAPDH). RESULTS: Experimental animals developed progressive proteinuria from 16 weeks onwards. At 8 weeks after IR injury, gene levels of matrix metalloproteinase (MMP) 2, an ECM-degrading enzyme, were significantly increased. Levels then fell progressively. This was associated with increasing expression of tissue inhibitor of metalloproteinases (TIMP) 1, an inhibitor of MMP-2, and of transforming growth factor (TGF) beta, a profibrotic cytokine, by 24 weeks following injury. CONCLUSION: These results suggest that, after an initial phase of increased ECM turnover following IR injury, the balance turns towards one of reduced degradation. This is likely to be an important mechanism in the subsequent development of fibrosis.
BACKGROUND: Cyclosporin is associated with significant chronic nephrotoxicity, manifest in the long term mainly as renal fibrosis. There have been claims that tacrolimus is a less fibrotic drug than cyclosporin, and this study was designed to determine the effect of the two drugs on the expression of fibrosis-associated genes. METHODS: Male Wistar rats underwent clamping of the right renal pedicle for 45 min together with left nephrectomy; this model has previously been shown to be associated with upregulation of fibrosis-associated genes. Experimental groups (six animals per group) received cyclosporin A 10 mg/kg daily, tacrolimus 0.2 mg/kg daily or no treatment. Animals were killed at 16 weeks, and the renal cortical expression of fibrosis-associated genes was studied by means of quantitative reverse transcriptase-polymerase chain reaction. RESULTS: Tacrolimus-treated animals developed significantly less proteinuria and had lower serum creatinine levels than those receiving cyclosporin. Tacrolimus administration also significantly reduced the expression of transforming growth factor beta and tissue inhibitor of metalloproteinases 1, both the products of genes associated with fibrosis. Although cyclosporin treatment reduced levels of the matrix-degrading enzymes, matrix metalloproteinase (MMP) 2 and MMP-9, this was not statistically significant. CONCLUSION: Tacrolimus has less nephrotoxicity than cyclosporin in this model. It also appears to have less fibrogenic potential, and this may have implications for the choice of long-term immunosuppressant in renal transplantation.
Mycobacteriophage Bxb1 is a temperate phage of Mycobacterium smegmatis. The morphology of Bxb1 particles is similar to that of mycobacteriophages L5 and D29, although Bxb1 differs from these phages in other respects. First, it is heteroimmune with L5 and efficiently forms plaques on an L5 lysogen. Secondly, it has a different host range and fails to infect slow-growing mycobacteria, using a receptor system that is apparently different from that of L5 and D29. Thirdly, it is the first mycobacteriophage to be described that forms a large prominent halo around plaques on a lawn of M. smegmatis. The sequence of the Bxb1 genome shows that it possesses a similar overall organization to the genomes of L5 and D29 and shares weak but detectable DNA sequence similarity to these phages within the structural genes. However, Bxb1 uses a different system of integration and excision, a repressor with different specificity to that of L5 and encodes a large number of novel gene products including several with enzymatic functions that could degrade or modify the mycobacterial cell wall.
Mycobacteriophage Bxb1 is a temperate phage of Mycobacterium smegmatis that shares a similar genome organization to mycobacteriophage L5, although the two phages are heteroimmune. We have investigated the regulatory circuitry of Bxb1 and found that it encodes a repressor, gp69, which regulates at least two promoters, an early lytic promoter, Pleft, and the divergent promoter, Pright. Bxb1 gp69 is 41% identical to the L5 repressor (gp71) and binds to repressor binding sites that conform to a similar, but distinct, 13 bp asymmetric consensus sequence to that for the L5 gp71 binding sites. The two phage repressors have a strong preference for their cognate binding sites, thus accounting for their immunity phenotypes. The Bxb1 genome contains 34 putative repressor binding sites located throughout the genome, but situated within short intergenic spaces and orientated in only one direction relative to the direction of transcription. Comparison with the locations of repressor binding sites within the L5 genome provides insights into how these unusual regulatory systems evolve.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A typical varicella zoster (ophthalmicus) in an incidentally HIV-infected person is reported in a young man. It was characterized by tense, grouped, vesiculobullous eruptions on a brick-red base. The diagnosis was substantiated by demonstration of swollen epidermal (balloon) cells with a nucleus/several nuclei containing inclusion bodies. Reticular degeneration was apparent.
Nail changes in Langerhans cell histiocytosis are distinctly uncommon. Paronychial erythema, swelling and subungual pustules of the fingernails and toenails were cardinal, and were supported by diffuse as well as dense collections of mononuclear Langerhans cells evidenced by microscopic investigation. Oral administration of co-trimoxazole (800 mg sulphamethoxazole + 160 mg trimethoprim) every 12 h, 50 mg/d cyclophosphamide and 80 mg/d predinisolone were the mainstay of treatment, supported by scalp tar shampoo and local betamethasone lotion application.
Patients who fail to attend initial appointments reduce clinic efficiency. To maximize attendance by newly referred outpatients, we introduced a mandatory group orientation clinic for all new patients and determined its effects on no-show rates. Orientation clinic also provided health care screening and opportunities for patient feedback. The new patient no-show rate for initial provider visits decreased significantly from 45% before institution of orientation clinic to 18% afterwards (P<.0001). The total no-show (patients who failed to attend orientation clinic or an initial provider visit) rate of the postintervention group was 51% (P = .28, compared with before the intervention). This intervention improved the efficiency and minimized the wasted time of our clinicians.