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Biomedical subjects

A Saxena

Publications and source records attributed to A Saxena.

At least 181 records · Page 10Linked to original sources
PubMed1995

Serial echocardiography for decision making in rapid two-stage arterial switch operation.

BACKGROUND: Rapid two-stage arterial switch operation is advocated in infants with simple transposition presenting late. Accurate assessment of left ventricular preparation is crucial to successful outcome. The role of echocardiography alone in surgical decision making remains unclear. METHODS: Seventeen patients with simple transposition (mean age, 4 months) underwent pulmonary artery banding and modified Blalock-Taussig shunt (first stage) to prepare the left ventricle for the arterial switch operation (second stage). Serial echocardiography was performed in the interval phase to assess left ventricular growth. Sixteen patients underwent arterial switch operation after a mean interval of 10.4 +/- 4 days, with 14 successful conversions. There was one mortality (5.9%) and two conversions to a Senning repair. RESULTS: In all patients a mean increase in left ventricular mass (40.8 +/- 17.8 g/m2 to 81.4 +/- 25.4 g/m2) and posterior wall thickness (3.37 +/- 0.47 mm to 4.63 +/- 0.58 mm) was recorded. Left ventricular end-diastolic internal diameter increased in all except the two switch failures. In all the successful cases the left ventricle had assumed a circular shape on cross-section with the interventricular septum contracting in synergy with the left ventricular mass. In the two failures, however, the interventricular septum had remained flat. CONCLUSIONS: Echocardiography can be used reliably in surgical decision making in rapid two-stage arterial switch operation. Increase in left ventricular mass, left ventricular posterior wall thickness, and left ventricular end-diastolic internal diameter toward normal combined with an acquisition of circular left ventricular configuration with the interventricular septum contracting in synergy with the left ventricular mass appear to best predict successful outcome.

Anastomosis, Surgical↗
PubMed1995

Results of mitral valve reconstruction in children with rheumatic heart disease.

BACKGROUND: Between January 1988 and November 1994, we developed techniques of reconstructing diseased mitral valves in patients with rheumatic heart disease. Four hundred thirteen patients underwent mitral valve repair using these techniques. Of these, 125 children and adolescents less than 15 years of age form the study group. METHODS: The mean age was 8.9 +/- 4.3 years (range, 5 to 15 years). One hundred seventeen patients (93.6%) had rheumatic heart disease. There were 72 boys (57.6%) and 53 girls (42.4%). All of these patients were symptomatic: New York Heart Association class III or IV. Mitral regurgitation alone was present in 49 patients (39.2%), and combined mitral stenosis and regurgitation were present in 76 patients (60.8%). Surgical techniques included commissurotomy (n = 70; 56%), annuloplasty (n = 122; 97.6%), chordal shortening (n = 46; 36.8%), cusp thinning (n = 27; 5.6%), and associated procedures for tricuspid valve disease (6 patients) and aortic valve disease (2 patients). RESULTS: The operative mortality rate was 4.8% (6 patients), and late deaths occurred in 1.6% (2 patients). Follow-up was 378.25 patient-years. In 15 patients, severe mitral regurgitation developed after a mean follow-up of 37.14 +/- 20.47 months (seven reoperations). At 6 years, actuarial and event-free survival rates were 92.1% +/- 3.19% and 75% +/- 8.18%, respectively. One patient (0.15%/patient-year) had transient right hemiparesis. None had anticoagulation-related bleeding. CONCLUSION: Mitral valve reconstruction in children and adolescents with rheumatic mitral regurgitation provides satisfactory early results. Progression of disease is the most important risk factor for reoperation. The technique described provided stable repair in the majority of patients.

Adolescent↗
PubMed1995

Characterization of monoclonal antibodies that inhibit the catalytic activity of acetylcholinesterases.

Monoclonal antibodies were generated against fetal bovine serum acetylcholinesterase and fetal bovine serum acetylcholinesterase inhibited by diisopropyl fluorophosphate or 7-(methylethoxyphosphinyloxy)-1-methylquinolinium iodide. Six monoclonal antibodies inhibited 70 to > 98% of the catalytic activity of fetal bovine serum acetylcholinesterase. Inhibition of serum acetylcholinesterase from several mammalia by four monoclonal antibodies showed broad cross-reactivity. In all cases, monoclonal antibodies bound to the native form of acetylcholinesterases. None reacted with serum butyrylcholinesterases from various species. Although all monoclonal antibodies inhibited catalytic activity of acetylcholinesterases, the site of interaction with acetylcholinesterase appeared to differ for several antibodies. Two types of acetylcholinesterase:monoclonal antibody complexes were formed: one between tetrameric forms and another between catalytic subunits within the tetramer. Monoclonal antibodies that inhibited acetylcholinesterase activity at > 98% also considerably slowed binding of diisopropyl fluorophosphate and other organophosphorus compounds to the acetylcholinesterase:monoclonal antibody complex. Binding of these monoclonal antibodies to acetylcholinesterase influenced function of the enzyme's peripheral anionic site. None of the antibodies bound to the esteratic site of acetylcholinesterase. Monoclonal antibodies caused changes in catalytic activity of acetylcholinesterase by interaction at a site remote from the catalytic site, presumably at the entrance to the active site gorge.

Acetylcholinesterase↗
PubMed1995

Systemic-to-pulmonary artery collateral vessels and surgical shunts in patients with cyanotic congenital heart disease: perioperative treatment by transcatheter embolization.

OBJECTIVE: Systemic-to-pulmonary collateral vessels can develop in patients with obstruction of the right ventricular outflow tract or the pulmonary artery. Occlusion of these vessels is necessary before surgical correction of the primary disease. We report the results of transcatheter coil embolization in the treatment of 56 patients. MATERIALS AND METHODS: Seventy-four procedures were done in the perioperative period for treatment of 67 aortopulmonary collateral arteries, five modified Blalock-Taussig shunts, and two enlarged veins. RESULTS: In the "aortopulmonary collateral" group, occlusion was complete in 51 patients (76%), subtotal in seven (10%), partial in four (6%), and failed in five (8%). Inadvertent embolization to the aorta occurred in two procedures, but both coils were retrieved nonsurgically. During follow-up of 1-12 months (n = 32; mean, 6.3 months), the coils remained in position, without any migration. Follow-up angiograms in 14 embolized vessels showed no recanalization (mean, 5.3 months; range, 2-12 months). In the "shunt" group, occlusion was complete in four patients and failed in one. Distal embolization to the pulmonary artery occurred in one patient. This coil was retrieved during surgery. During follow-up of 3-6 months, coils remained in position in all patients. In one patient, a follow-up angiogram at 3 months showed no recanalization. In the "venous embolization" group, occlusion was complete in one patient. The coils were in position 5 months later. The procedure was unsuccessful in the other patient. CONCLUSION: We conclude that transcatheter coil embolization is useful in the treatment of abnormal systemic-to-pulmonary vessels and shunts in patients with obstruction of the right ventricular outflow tract or the pulmonary artery. Homemade coils are safe and effective in obliterating antegrade flow.

Adolescent↗
PubMed1995

An epidemiological study of prevalence of pain in head & neck cancers.

This study was undertaken on 117 consecutive patients referred to a head and neck oncology clinic at a major hospital in New Delhi. 89.5 per cent patients were in clinical stage III or IV at the time of referral. The prevalence of pain was 83.8 per cent with a mean pain duration of 6.2 +/- 5.9 months and a mean pain intensity of 5.0 +/- 2.7 on a modified numerical rating scale ranging from 0 to 10. The mean intensity of pain was not significantly different for age groups or stage of the disease but patients with oro-pharyngeal cancers had significantly higher pain scores than patients with hypopharyngeal cancers (4.6 +/- 3.0 vs 2.9 +/- 2.5, P < 0.05).

Adolescent↗
PubMed1995

Significance of left ventricular inflow gradients in patients with ventricular septal defect.

Hemodynamic data of 167 patients of isolated ventricular septal defect (VSD) was retrospectively analyzed for the presence of left ventricular inflow gradients. End diastolic gradients of > 5 mm Hg between the pulmonary artery wedge pressure and the left ventricular end diastolic pressure were recorded in 40 of these patients. In three of these cases, left atrium was also entered and identical pressure gradients were recorded between the left atrial pressure and the left ventricular end diastolic pressure. Two dimensional and Doppler echocardiographic or operative findings were available in 32 of the 40 patients. No statistical correlation was found between the presence and degree of left ventricular inflow gradients at end diastole and the degree of left to right shunt. Out of a total of 40 patients with left ventricular inflow gradients, gradients of 6-10 mm Hg were present in 24 patients. Echocardiographic or operative findings available in 19 of these did not show any left ventricular inflow obstruction. Enddiastolic gradients of 11-15 mm Hg were present in 14 patients. Echocardiographic or operative findings were available in 11 of these and one of these had congenital mitral stenosis at surgery. End diastolic gradients of more than 15 mm Hg were present in 2 patients and one of these had congenital mitral stenosis at surgery. Thus organic left ventricular inflow obstruction is rare with inflow mitral gradients of upto 15 mm Hg in patients of VSD.

Adolescent↗
PubMed1994

The asialoglycoprotein receptor is associated with a tyrosine kinase in HepG2 cells.

The asialoglycoprotein (ASGP) receptor undergoes constitutive endocytosis in HepG2 cells, which is regulated by tyrosine kinase activity (Fallon, R. J., Danaher, M., Saylors, R. L., and Saxena, A. (1994) J. Biol. Chem. 269, 11011-11017). In this study we show that the receptor copurifies with a tyrosine kinase activity, as defined by tyrosine phosphorylation of an exogenous substrate (reduced carboxyamidomethylated and maleylated lysozyme). Analysis of cells transfected with one subunit of the ASGP receptor showed that signals in the cytoplasmic domain of the H1 subunit are sufficient for receptor kinase association. In addition, receptor kinase association is not dependent on the single cytoplasmic tyrosine at position 5. Analysis of the components of anti-ASGP receptor immunoprecipitates revealed the presence of a 127-kDa protein (p127), which becomes phosphorylated on tyrosine upon addition of gamma-[32P]ATP and which is capable of binding ATP.p127 was also demonstrated in anti-transferrin receptor immunoprecipitates but not in immunoprecipitates of a resident membrane protein, human HLA. In conclusion, these data demonstrate that the ASGP receptor, a protein that participates in constitutive, rapid endocytosis, is associated with a cellular tyrosine kinase.

Asialoglycoprotein Receptor↗
PubMed1994

Defective asialoglycoprotein receptor endocytosis mediated by tyrosine kinase inhibitors. Requirement for a tyrosine in the receptor internalization signal.

Regulated endocytosis by growth factor receptors requires intact receptor-associated tyrosine kinase activity. To determine whether a similar requirement exists for the asialoglycoprotein (ASGP) receptor which lacks intrinsic tyrosine kinase activity and participates in constitutive endocytosis, we examined the effect of three tyrosine kinase inhibitors, tyrphostin, genistein, and staurosporine, on receptor-mediated endocytosis in the human hepatoma line HepG2. These compounds inhibited early receptor internalization from the plasma membrane to internal protease-resistant sites in a concentration-dependent manner. This effect correlated with their inhibition of tyrosine phosphorylation of the ASGP receptor in vitro. Receptor trafficking subsequent to receptor internalization was unaffected. Endocytosis of another constitutively internalized protein, the transferrin receptor, was also inhibited by these compounds. In contrast, pinocytosis of the fluid-phase marker Lucifer yellow was not inhibited. The tyrosine kinase inhibitors also decreased the endocytic rate of transfected ASGP receptor H1 subunit in SK-Hep-1 cells. Therefore an intact ASGP receptor heterooligomeric complex is not required for this effect. Mutation of the single cytoplasmic tyrosine at position 5 of the H1 subunit to phenylalanine produced an ASGP receptor which was endocytosed regardless of treatment with the tyrosine kinase inhibitors. We conclude that tyrosine kinase activity modulates the rate of receptor endocytosis at a point early in the internalization process.

Adenosine Triphosphate↗
PubMed1994

Heterogeneity of subcellular localization of p53 protein in human glioblastomas.

Immunohistochemical analysis of the p53 protein in human glioblastomas with known genetic profiles of p53 mutations and allele losses on chromosome 17p demonstrated a heterogeneous pattern of subcellular compartmentalization of the p53 protein. Tumors with a single wild type copy of the p53 gene but with allelic deletions on chromosome 17p exhibit nuclear and/or cytoplasmic accumulation of p53, whereas tumors with both copies of the wild type gene and no allele losses on chromosome 17 do not accumulate p53. Glioblastomas with one normal and one mutated copy of the p53 gene and allelic deletions on 17p distal to p53, on the other hand, show predominantly cytoplasmic staining, probably originating from the wild type p53 protein. Furthermore, tumors with mutations in the same codon of p53 display quite different intracellular distribution suggesting that, in addition to the genotype of p53, the intracellular microenvironment of a particular tumor is important in determining the subcellular localization of the p53 protein.

Base Sequence↗