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P Sampathkumar

Publications and source records attributed to P Sampathkumar.

11 recordsLinked to original sources
PubMed2001

Fusarium infection after solid-organ transplantation.

We describe a case of soft tissue infection caused by Fusarium species in a heart-liver transplant recipient, and review the cases of fusarial infection reported among solid-organ transplant (SOT) recipients. Unlike fusarial infection in patients with hematologic malignancies or bone marrow transplants, fusarial infection in SOT recipients tends to be localized, occurs later in the posttransplantation period, and has a better outcome. Surgical resection, when possible, and prolonged treatment with amphotericin provide the most effective form of therapy.

Amphotericin B↗
PubMed2000

Prosthetic joint infection due to Staphylococcus lugdunensis.

Staphylococcus lugdunensis, a coagulase-negative staphylococcus, is being increasingly recognized as the cause of serious infections. We report 2 cases of total knee arthroplasty infection caused by S lugdunensis. S lugdunensis frequently produces a clumping factor that can result in a positive slide (short) coagulase test result. If the microbiology laboratory does not use the tube coagulase (long) test to confirm the slide coagulase test result, the organism may be misidentified as Staphylococcus aureus. S lugdunensis is more virulent than other coagulase-negative staphylococci and in many clinical situations behaves like S aureus, further increasing the confusion. However, S lugdunensis differs from S aureus in that it is susceptible to most antibiotics. This fact may alert the microbiology laboratory or the clinician that the isolate is likely not S aureus and prompt further testing of a specific isolate. Accurate identification of S lugdunensis isolates facilitates studies to define the epidemiology and pathogenesis of prosthetic joint infection due to S lugdunensis and delineates optimal medical and surgical therapies.

Aged↗
PubMed1998

Post-liver transplantation myocardial dysfunction.

Patients with end-stage liver disease usually show a hyperdynamic circulatory state. It has previously been reported that patients who develop myocardial depression in the early post-liver transplantation period are more prone to organ failure and death. We reviewed the records of 754 adult patients undergoing liver transplantation at our institution and identified 7 patients who initially showed hyperdynamic circulation, but then developed reversible dilated cardiomyopathy in the early posttransplantation period. All identifiable causes of cardiac dysfunction, such as myocardial ischemia, thyroid dysfunction, and electrolyte imbalances, were excluded. Left ventricular ejection fraction decreased from a preoperative median baseline of 60% to 20% (P = .02), with four-chamber dilatation on echocardiogram. All these patients required supportive care, including mechanical ventilation, afterload reduction, inotropic support, and monitoring in the intensive care unit. Cardiac function subsequently improved in all patients, with ejection fraction increasing to a median of 50%. All patients were discharged from the hospital. At a median follow-up of 15 months, there was no recurrence of heart failure. The increased peripheral resistance seen after successful liver transplantation may be an important causative factor.

Adolescent↗
PubMed1988

Microbiological and clinical effects of chlorhexidine digluconate and hydrogen peroxide mouthrinses on developing plaque and gingivitis.

While the ability of chlorhexidine (CHX) to prevent plaque formation and inhibit the development of gingivitis has been well documented in the literature, the therapeutic value of hydrogen peroxide (H2O2) in preventing gingivitis is in dispute. The purpose of this study was to compare the clinical and microbiological effects of an established therapeutic agent, such as chlorhexidine with that of H2O2 in the experimental gingivitis model. Following a period of stringent oral hygiene, 32 subjects were allocated to 1 of 3 treatment groups which were balanced on the basis of their pre-experimental gingivitis scores. The subjects then refrained from any oral hygiene for 21 days. During this period, they rinsed twice a day with either a placebo, 0.12% CHX, or a 1% H2O2 mouthrinse. After 21 days, supragingival and marginal plaque was collected from each subject and assayed for total cultivable microbiota, total facultative anaerobes, facultative Streptococci, Actinomyces, Fusobacterium, Veillonella and Capnocytophaga. At the end of the experimental period, the group rinsing with 0.12% CHX showed 95% reduction in gingivitis incidence, 100% reduction in bleeding sites, and 80% reduction in plaque scores compared to the group rinsing with placebo. Conversely, the group using 1% H2O2 showed a marginal reduction in gingivitis incidence of 15% and a 28% reduction in bleeding sites compared to the placebo group, but no significant reduction in plaque scores. The microbiological results showed that 0.12% CHX was an excellent broad-spectrum antimicrobial agent which significantly reduced the number of both facultative and obligate anaerobes in plaque.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacteria↗
PubMed1985

Transcription of the replication control region of the IncFII R-plasmid NR1 in vitro and in vivo.

The minimal replicon of the 90,000 base-pair IncFII R plasmid NR1 consists of a 2700 base-pair region of the DNA. Minireplicator plasmids consisting of the 2700 base-pair minimal replicon plus a 2200 base-pair region coding for chloramphenicol acetyltransferase (cat) were used as templates for in vitro transcription. Six RNA transcripts were synthesized from these templates in vitro. We have determined the directions of transcription and the approximate sites of initiation and termination of each of the in vitro RNA transcripts. One RNA transcript was synthesized from the cat gene, while the other five were transcribed from the minimal replicon. Four of the RNA transcripts also were identified by quantitative hybridization of RNA synthesized in vivo from these minireplicator plasmids. The strengths of the promoters for the RNA transcripts were estimated by the relative rates of transcription both in vitro and in vivo. Transcription from convergent promoters reduced the rate of RNA synthesis in vivo in both directions. In vivo, a significant fraction of the cat mRNA was extended past its in vitro termination point. Transcription of mutants that have altered plasmid copy number and/or incompatibility properties also were examined. The possible roles of each of the transcripts as mRNA and their involvement in regulation of DNA replication are discussed.

Base Sequence↗
PubMed1982

Chorismate mutase-prephenate dehydrogenase from Escherichia coli. Purification and properties of the bifunctional enzyme.

A pure, stable preparation of chorismate mutase-prephenate dehydrogenase (chorismate pyruvatemutase, EC 5.4.99.5-prephenate:NAD+ oxidoreductase (decarboxylating), EC 1.3.1.12) has been obtained in good yield from a regulatory mutant of Escherichia coli. The enzyme was purified from extracts of the organism by treatment with streptomycin sulfate and fractionation with ammonium sulfate followed by chromatography on columns of Sepharose-AMP, DEAE-cellulose and hydroxyapatite. The native enzyme has a molecular weight of 88,000 and is made up of two identical subunits as indicated by the results of amino acid composition, peptide mapping and electrophoresis in the presence of sodium dodecyl sulfate. The enzyme has a sedimentation coefficient of 4.85 S as determined in the ultracentrifuge and an isoelectric point of pH 5.3. Preliminary studies on the kinetic properties of the enzyme indicated that both the mutase and the dehydrogenase reactions catalyzed by the enzyme conform to Michaelis-Menten kinetics.

Amino Acids↗
PubMed1982

Chorismate mutase-prephenate dehydrogenase from Escherichia coli. Kinetic mechanism of the prephenate dehydrogenase reaction.

The mechanism of the dehydrogenase reaction catalyzed by chorismate mutase-prephenate dehydrogenase (chorismate pyruvatemutase, EC 5.4.99.5-prephenate:NAD+ oxidoreductase (decarboxylating), EC 1.3.1.12) has been investigated using steady-state kinetic techniques. The steady-state velocity pattern in the absence of products as well as product and dead-end inhibition patterns are consistent with a random mechanism in which two dead-end complexes, E-NADH-prephenate and E-NAD-hydroxyphenylpyruvate, are formed, and in which all steps are in rapid equilibrium except that concerned with the interconversion of central ternary complexes. Values have been determined for the maximum velocity of the reaction as well as for the kinetic parameters associated with the combination of substrates, products and the dead-end inhibitor, AMP, with various enzyme forms. The results indicate that when albumin is present in the reaction mixture, the presence of one substrate on the enzyme does not affect the combination of the second substrate. On the other hand, the binding of 4-hydroxyphenylpyruvate is enhanced by the presence of NAD and the binding of NADH is enhanced by the presence of prephenate on the enzyme. These results contrast with the finding that the inhibitory analogue, AMP, binds more strongly to the free enzyme than to the E-prephenate complex.

Adenosine Monophosphate↗