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Biomedical subjects

M Chidambaram

Publications and source records attributed to M Chidambaram.

At least 19 recordsLinked to original sources
PubMed2006

Limitations of a PI controller for a first-order nonlinear process with dead time.

A nonlinear process, the conical tank level process whose parameters vary with respect to the process variable, is considered. The time constant and gain of the chosen process vary as a function of level. A deliberate dead time is introduced in the system by delaying the valve opening. The limitations of the conventional PI controller tuned using Ziegler-Nichols settings for the chosen process are brought out. The servo and regulatory responses through simulation and experimentation for various magnitudes of set-point changes and load changes at various operating points with the controller tuned only at a chosen nominal operating point are obtained and analyzed. Regulatory responses for output load changes are studied. A benchmark system is presented to understand clearly how variations of system parameters affect the performance of the controller. A gain scheduled controller is proposed to handle the control problem. Present work illustrates the simplicity and effectiveness of the gain scheduling.

Journal Article↗
PubMed2005

Design of controller using variable transformations for a nonlinear process with dead time.

In this work, a globally linearized controller (GLC) for a first-order nonlinear system with dead time is proposed. This is similar to the GLC proposed by Ogunnalke [Ind. Eng. Chem. Process. Des. Dev. 25, 241-248 (1986)] for nonlinear systems without dead time. Two methods are proposed. One is based on the Smith prediction from the model in the transformed domain and the other is based on Newton's extrapolation method. The simulation study is made on the conical tank level process and the results are compared with those obtained using a conventional PI controller and the Smith PI controller based on the transfer function model about the operating point 39%. Finally, experimental results on the laboratory conical tank level process are also given.

Journal Article↗
PubMed2002

Type I membranoproliferative glomerulonephritis in an HIV-infected individual without hepatitis C co-infection.

Type I membranoproliferative glomerulonephritis (MPGN) is an uncommon manifestation of human immunodeficiency virus (HIV)-associated renal disease in patients co-infected with hepatitis C virus (HCV). We describe a case of Type I MPGN in an HIV-positive diabetic man with nephrotic-range proteinuria and renal insufficiency who was not co-infected with HCV. Tubuloreticular inclusions were present but there was no evidence for either cryoglobulinemia or cryoglobulin deposits in the kidney. This finding suggests that Type I MPGN may represent a reaction of the kidney to HIV independent of the effects of HCV co-infection. Clinical suspicion must be maintained for Type I MPGN in all HIV infected patients presenting with significant proteinuria regardless of HCV infection status.

AIDS-Associated Nephropathy↗
PubMed1998

Complete genome sequence of Treponema pallidum, the syphilis spirochete.

The complete genome sequence of Treponema pallidum was determined and shown to be 1,138,006 base pairs containing 1041 predicted coding sequences (open reading frames). Systems for DNA replication, transcription, translation, and repair are intact, but catabolic and biosynthetic activities are minimized. The number of identifiable transporters is small, and no phosphoenolpyruvate:phosphotransferase carbohydrate transporters were found. Potential virulence factors include a family of 12 potential membrane proteins and several putative hemolysins. Comparison of the T. pallidum genome sequence with that of another pathogenic spirochete, Borrelia burgdorferi, the agent of Lyme disease, identified unique and common genes and substantiates the considerable diversity observed among pathogenic spirochetes.

Bacterial Proteins↗
PubMed1996

Epidemiology of Staphylococcus aureus during space flight.

Staphylococcus aureus was isolated over 2 years from Space Shuttle mission crewmembers to determine dissemination and retention of bacteria. Samples before and after each mission were from nasal, throat, urine, and feces and from air and surface sampling of the Space Shuttle. DNA fingerprinting of samples by digestion of DNA with SmaI restriction endonuclease followed by pulsed-field gel electrophoresis showed S. aureus from each crewmember had a unique fingerprint and usually only one strain was carried by an individual. There was only one instance of transfer between crewmembers. Strains from interior surfaces after flight matched those of crewmembers, suggesting microbial fingerprinting may have forensic application.

DNA Fingerprinting↗
PubMed1996

Sensitization of bacteria to danofloxacin by temperate prophages.

Danofloxacin (CP-76,136) is in a class of agents that inhibit DNA gyrase and trigger induction of the SOS response and temperate bacteriophages. Killing studies against the bovine pathogen Pasteurella haemolytica demonstrated that danofloxacin exhibits particularly rapid killing kinetics. Here, lysogenic Escherichia coli bearing lambda is found to be more sensitive to danofloxacin than nonlysogenic E. coli. Danofloxacin exposure also induced a prophage in P. haemolytica. The potency of danofloxacin against lysogens in likely enhanced by this prophage induction.

Animals↗
PubMed1996

Increased production of colicin E1 in stationary phase.

The synthesis of colicin E1 is known to be regulated by the SOS response, anaerobiosis, and catabolite repression. The expression of cea-lacZ fusions was also found to be stimulated when cells reached stationary phase. This increase in expression was determined to be due to depletion of nutrients from the medium, since the addition of fresh medium reversed the effect. Expression of the fusion increased when cells were starved in 10 mM MgSO4 and when they were grown in conditioned medium in which cells had been grown previously. The stimulation of expression occurred when the cea-lacZ fusion was present in single-copy as well as in multicopy plasmids. Finally, the data were consistent with this increase being independent of the SOS response, anaerobiosis, catabolite repression, and integration host factor as well as the stationary-phase regulators encoded by rpoS and lrp.

Bacteria↗
PubMed1995

Isolation of Pasteurella haemolytica leukotoxin mutants.

Two mutants of Pasteurella haemolytica A1 that do not produce leukotoxin were isolated. Following mutagenesis, colonies were screened with antiserum by a filter assay for absence of the secreted leukotoxin. The two mutants both appeared to produce normal amounts of other antigens, as judged by reactivity with polyclonal serum from an animal with pasteurellosis, and were not altered in beta-hemolytic activity as seen on blood agar plates. There was no evidence of either cell-associated or secreted leukotoxin protein when Western blots (immunoblots) were carried out with the polyclonal serum or with a monoclonal antibody directed against the leukotoxin. Southern blots revealed that both mutants show the wild-type restriction pattern at the leukotoxin locus, although the strain with the lktA2 mutation showed differences in other regions of the chromosome on analysis by pulsed-field gel electrophoresis. The strain with the lktA2 mutation grew more slowly than did the wild-type strain, while the strain with the lktA1 mutation was indistinguishable from the wild-type strain in its growth properties. The strain with the lktA1 mutation should be valuable in determining the role of the leukotoxin in virulence as well as in identifying other virulence factors of P. haemolytica.

Bacterial Toxins↗
PubMed1995

Antigenic and virulence properties of Pasteurella haemolytica leukotoxin mutants.

Antigenic properties of two mutants of Pasteurella haemolytica, strains 59B0071 and 59B0072, that do not produce detectable leukotoxin were investigated. Western blot (immunoblot) analysis with a number of polyclonal sera from animals recovering from pasteurellosis revealed that both mutants secreted a variety of antigens that were also present in cultures of several wild-type strains. These antigens ranged from about 100 to 15 kDa. Mutant strain 59B0071 was found to be totally deficient in leukotoxin, as judged not only by Western blotting but also by cytotoxicity assays with bovine lymphoma (BL-3) cells or bovine polymorphonuclear cells as targets. The mutant strain 59B0071 had normal levels of a secreted sialylglycoprotease, however. When strains were tested for virulence in goat and cattle challenge experiments, a reduction in mortality and lung lesions was observed with the mutant 59B0071 in comparison with results obtained with wild-type strains. These results are consistent with an important role for leukotoxin in P. haemolytica virulence and suggest that leukotoxin-negative mutants may be useful tools in the investigation of other virulence properties involved in P. haemolytica infections.

Animals↗
PubMed1995

DNA repair mutants of Rhodobacter sphaeroides.

The genome of the photosynthetic eubacterium Rhodobacter sphaeroides 2.4.1 comprises two chromosomes and five endogenous plasmids and has a 65% G+C base composition. Because of these characteristics of genome architecture, as well as the physiological advantages that allow this organism to live in sunlight when in an anaerobic environment, the sensitivity of R. sphaeroides to UV radiation was compared with that of the more extensively studied bacterium Escherichia coli. R. sphaeroides was found to be more resistant, being killed at about 60% of the rate of E. coli. To begin to analyze the basis for this increased resistance, a derivative of R. sphaeroides, strain 2.4.1 delta S, which lacks the 42-kb plasmid, was mutagenized with a derivative of Tn5, and the transposon insertion mutants were screened for increased UV sensitivity (UVs). Eight UVs strains were isolated, and the insertion sites were determined by contour-clamped homogeneous electric field pulsed-field gel electrophoresis. These mapped to at least five different locations in chromosome I. Preliminary analysis suggested that these mutants were deficient in the repair of DNA damage. This was confirmed for three loci by DNA sequence analysis, which showed the insertions to be within genes homologous to uvrA, uvrB, and uvrC, the subunits of the nuclease responsible for excising UV damage.

Amino Acid Sequence↗
PubMed1992

Relationship of atrial fibrillation to significant pericardial effusion in valve-replacement patients.

Rhythm change was observed in 21 of 242 (8.7%) patients during the first four weeks of open heart surgery (OHS). In the valve-replacement group of 148 patients the rhythm change was found to be associated with significant pericardial effusion (PE). Seven patients had rhythm changes during the first three days of OHS unrelated to PE. Two patients who were in atrial fibrillation (AF) developed fast ventricular rate and twelve patients showed rhythm change from sinus to supraventricular tachyarrhythmia (AF in ten and supraventricular tachycardia in two) and all these fourteen patients had significant PE. With pericardiocentesis or open drainage or withdrawal of anticoagulation, AF reverted to sinus rhythm in nine patients and five patients remained in AF but with a slow ventricular rate. Significant PE was related to a high anticoagulation ratio. We conclude from this study that within the first four weeks of OHS, high anticoagulation ratio contributes to the development of significant PE, and tachyarrhythmia (particularly AF) is a forerunner of significant PE or cardiac tamponade: the aim of management should be to rule out or show evidence of significant PE once tachyarrhythmia develops, and if significant PE is present then the pressure in the pericardial cavity should be reduced.

Atrial Fibrillation↗
PubMed1989

Fine structure genetic and physical map of the phage P22 tail protein gene.

Bacteriophage P22 which are incapable of making functional tail protein can be propagated by the addition of purified mature tail protein trimers to either liquid or solidified medium. This unique in vitro complementation condition has allowed us to isolate 74 absolute lethal tail protein mutants of P22 after hydroxylamine mutagenesis. These phage mutants have an absolute requirement for purified P22 tail protein to be present in a soft agar overlay in order to form plaques and do not grow on any nonsense suppressing strains of Salmonella typhimurium. In order to genetically map and physically locate these mutations we have constructed two complementary sets of fine structure deletion mapping strains using a collection of Tn1 insertions in gene 9, the structural gene for the tail protein. Fourteen bacteriophage P22 strains carrying unique Tn1 transposon insertions (Ap phage) in gene 9 have been crossed with Ap phage carrying Tn1 insertions in gene 20. Phage carrying deletions that arose from homologous recombination between the Tn1 elements were isolated as P22 lysogens. The deletion prophage were shown to be missing all genetic information bracketed by the parental Tn1 elements and thus form a set of deletions into gene 9 from the 5' end of the gene. From the frequency of production of these deletion phage the orientation of the Tn1 insertions in gene 9 could be deduced. The genetic end points of the deletions in gene 9 and thus the order of Tn1 insertions were determined by marker rescue experiments using the original Ap phage. The genetic end points of the deletions in gene 20 were determined in similar experiments using nonsense mutations in gene 20. To locate the physical end points of these deletions in gene 9, DNA containing the Tn1 element has been cloned from each of the original Ap phage into plasmids. The precise point of insertion of Tn1 into gene 9 was determined by restriction enzyme mapping and DNA sequencing of the relevant portions of each of these plasmids. In vitro deletion of different 3' gene 9 sequences in the plasmid clones was accomplished through the use of unique restriction endonuclease sites in Tn1. The resulting plasmids form a set of deletions extending into the 3' end of the gene which are complementary compared to the deletion lysogens.(ABSTRACT TRUNCATED AT 400 WORDS)

Chromosome Mapping↗
PubMed1987

Long-term results of DeVega tricuspid annuloplasty.

DeVega tricuspid annuloplasty was performed in 74 patients undergoing mitral or mitral and aortic valve replacement between January, 1972, and December, 1985. Sixty-two hospital survivors have been followed up for a mean of 85.3 +/- 6.6 months. Actuarial survival at 14 years was 71.5 +/- 8.2%. None of the late deaths was related to the tricuspid annuloplasty. Three patients required tricuspid valve replacement for recurrence of tricuspid regurgitation (0.68% per annum). Eleven asymptomatic patients studied hemodynamically at a mean period of 53 months after the operation showed maintenance of the hemodynamic improvement. We recommend DeVega annuloplasty as the method of choice for moderate to severe tricuspid regurgitation in the absence of an organically diseased or deformed valve.

Adolescent↗
PubMed1984

Durability of the pericardial valve.

The fate of 1001 pericardial xenograft valves was analysed during a maximum follow-up period of 13 years. Two basic types of pericardial valves have been implanted. Between 1971 and 1975, 213 patients received 'hospital made' valves (single replacement). Between 1976 and 1983, 601 patients received 788 pericardial valves manufactured by Shiley Inc. (474 Standard and 314 Low profile valves) for both single and multiple replacement. There were 27 instances of valve dysfunction between 13 and 92 months after operation, 20 with 'hospital made' and 7 with Shiley valves. The actuarial freedom from valve failure at 8 years is 94.0 +/- 4.6% for aortic and 98.8 +/- 1.2% for mitral replacement in patients with Shiley valves. In patients with 'hospital made' valves the actuarial freedom from valve failure at 12 years of follow-up is 86.7 +/- 7.6% for aortic and 84.7 +/- 14.1% for mitral replacement. The linearised rate of valve dysfunction was 0.31% per annum for Shiley valves and 1.27% per annum for 'hospital made' valves. This analysis demonstrates that the pericardial xenograft has a low risk of valve failure and a predictable behaviour over a period of 13 years. The Shiley made valves have shown improved durability when compared with the 'hospital made' valves.

Adolescent↗
PubMed1983

Isolation and characterization of precursors in bacteriophage T4 baseplate assembly. II. Purification of the protein products of genes 10 and 11 and the in vitro formation of the P(10/11) complex.

Two bacteriophage T4 proteins which are precursors to the phage baseplate have been purified to homogeneity. These proteins, P10 and P11, are components of the P(10/11) complex, which is the first intermediate in the assembly of T4 baseplate 1/6th arms. Each protein was isolated from cells infected with a T4 amber mutant defective in the production of the other protein. Thus these purified proteins have never been assembled into the P(10/11) complex in vivo. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis and the ability of these proteins to block the phage killing activity of specific antisera were used to monitor the purification steps. Sedimentation equilibrium experiments reveal a molecular weight of 188,000 g/mol for P10 and 60,000 g/mol for P11. These data together with the previously determined molecular weights of the gene 10 and gene 11 polypeptide chains (King & Mykolajewycz, 1973) and the in vivo assembled P(10/11) complex (Berget & King, 1978b) are consistent with P10 being a dimer of the product of gene 10, P11 being a dimer of the product of gene 11, and P(10/11) being a tetramer containing one of each of these dimers. Purified P10 and P11 are active in assembly because they complement 10- and 11- defective extracts, respectively, to form viable bacteriophage in vitro. Furthermore, these proteins assemble in vitro to form a protein structure identical to the P(10/11) complex formed in vivo as determined by non-denaturing gel electrophoresis. This P(10/11) complex formed in vitro complements 10-/11- defective extracts to form viable phage. The overall extent of this in vitro assembly reaction is not affected by NaCl to 1.5 M or 2% Triton X-100. The reaction is, however, prevented by the denaturing effects of urea and sodium dodecyl sulfate.

Antibodies↗
PubMed1982

Clinical durability of the pericardial xenograft valve: ten years experience with mitral replacement.

Data from 366 patients with mitral valve replacement (250 single and 116 multiple) who received pericardial xenografts between 1971 and 1981 were analyzed. Cumulative duration of follow-up was 1,151 patient-years, with a maximum duration of 10.7 years. Actuarial survival at 11 years is 71.6 +/- 14.2%. Pericardial valve failure occurred in 7 patients (0.6 episodes per 100 patient-years). Actuarial freedom from valve failure at 11 years is 90.4 +/- 9.1% for the entire series. Although 275 (75.1%) patients were in chronic atrial fibrillation, anticoagulants were not used in any patient beyond the first 6 postoperative weeks. The incidence of emboli was 0.6% per year. Six episodes occurred following single mitral valve replacement and 1 after multiple valve replacement (5 early and 2 late). The actuarial freedom from embolism in 96.4 +/- 1.5% at 6 and 11 years postoperatively. Valve thrombosis has not been encountered. This analysis has shown a low incidence of valve dysfunction and a very low risk of embolic complications without long-term anticoagulation. The pericardial xenograft is a safe substitute for the mitral valve, with predictable behavior during the first decade of follow-up.

Adolescent↗