Systemic venous collateral development after the bidirectional cavopulmonary anastomosis. Prevalence and predictors

OBJECTIVES: To determine the prevalence of systemic venous collaterals after the bidirectional cavopulmonary anastomosis and the factors associated with their development. BACKGROUND: Systemic venous collaterals have been found after cavopulmonary anastomosis. Methods. Cardiac catheterization was performed in 103 patients before and after a bidirectional cavopulmonary anastomosis. RESULTS: After surgery, 51 venous collaterals were identified in 32 patients (31%). Collateral development was associated with an abnormal superior vena caval connection (56% incidence vs. 26% with a single right superior vena cava, p = 0.01) and postoperative factors including pulmonary artery distortion (53% incidence vs. 22% without distortion, p = 0.002); increased superior vena caval mean pressure (14 +/- 5 mm Hg versus 11 +/- 4 mm Hg with no collaterals, p = 0.0002); increased pulmonary artery mean pressure (13 +/- 4 mm Hg vs. 11 +/- 4 mm Hg with no collaterals, p = 0.02); lower right atrial mean pressure (5 +/- 2 mm Hg vs. 6 +/- 3 mm Hg with no collaterals, p = 0.04); and increased mean gradient between superior vena cava and right atrium (8 +/- 3 mm Hg vs. 5 +/- 4 mm Hg with no collaterals, p = 0.0002). Using multiple logistic regression, only this last factor was independently associated with collateral development with an odds ratio per 1 mm Hg of 1.33 (95% CI 1.12-1.58, p = 0.001) for their presence. CONCLUSIONS: Systemic venous collaterals occur frequently after a bidirectional cavopulmonary anastomosis and are found postoperatively when a significant pressure gradient occurs between cava and right atrium.     

Comparative analysis of breast cancer contamination in mobilized and nonmobilized hematopoietic grafts

We report a case of an 18-month-old female who presented with three supernumerary upper limbs of varying lengths on the right side. Each limb had a proximal, middle, and distal segment, and an intercalated elbow and wrist joint. A single digit was present in the superior limb, three digits in the middle limb, and two digits in the caudal-most limb. Right plagiocephaly, congenital torticollis, scoliosis involving the upper and mid thoracic region, and a hypoplastic right pectoralis major were the other abnormal features noted. Radiography showed two scapulae, humerus, a single forearm bone in each limb, and rudimentary metacarpals and phalanges. Limb duplication may rarely be encountered in parasitic conjoined twins. The role of mutagens, drugs, cellular contributions, and morphogens in the growth and differentiation of limbs has been studied in animals. It is rather difficult to deduce the time of action of the factors responsible for such a malformation.     

Structure-activity analysis of the interaction of curacin A, the potent colchicine site antimitotic agent, with tubulin and effects of analogs on the growth of MCF-7 breast cancer cells

Originally purified as a major lipid component of a strain of the cyanobacterium Lyngbya majuscula isolated in Cura?ao, curacin A is a potent inhibitor of cell growth and mitosis, binding rapidly and tightly at the colchicine site of tubulin. Because its molecular structure differs so greatly from that of colchicine and other colchicine site inhibitors, we prepared a series of curacin A analogs to determine the important structural features of the molecule. These modifications include reduction and E-to-Z transitions of the olefinic bonds in the 14-carbon side chain of the molecule; disruption of and configurational changes in the cyclopropyl moiety; disruption, oxidation, and configurational reversal in the thiazoline moiety; configurational reversal and substituent modifications at C13; and demethylation at C10. Inhibitory effects on tubulin assembly, the binding of colchicine to tubulin, and the growth of MCF-7 human breast carcinoma cells were examined. The most important portions of curacin A required for its interaction with tubulin seem to be the thiazoline ring and the side chain at least through C4, the portion of the side chain including the C9-C10 olefinic bond, and the C10 methyl group. Only two modifications totally eliminated the tubulin-drug interaction. The inactive compounds were a segment containing most of the side chain, including its two substituents, and analogs in which the methyl group at the C13 oxygen atom was replaced by a benzoate residue. Antiproliferative activity comparable with that observed with curacin A was only reproduced in compounds that were potent inhibitors of the binding of colchicine to tubulin. Molecular modeling and quantitative structure-activity relationship studies demonstrated that most active analogs overlapped extensively with curacin A but failed to provide an explanation for the apparent structural analogy between curacin A and colchicine.     

Idiopathic pulmonary haemosiderosis--a case report

Nurse educators regularly develop clinical learning experiences for undergraduate students using the expertise of experienced RNs as preceptors. Preceptors help students develop a knowledge base and clinical skills. This article reports a literature review and summarizes the benefits of preceptorship, outlines preceptor responsibilities and qualities, and discusses the process of preceptor selection and role preparation. Suggestions for collaborative efforts regarding the preceptor experience among staff nurses, nurse educators, and staff development educators are highlighted.     

O-ethyl 14C]phenacetin O-deethylase activity in human liver microsomes

The activity of human liver microsomal cytochrome P450 1A2 (CYP1A2) is readily estimated by following the O-deethylation of [O-ethyl 14C]phenacetin (PODase). The basis of the assay is the quantitative measurement of [14C]acetaldehyde, remaining in the supernatant of assay incubates, after extraction of unmetabolized [O-ethyl 14C]phenacetin with charcoal. In the presence of native human liver microsomes (K(m) = 54 +/- 27 microM; V(max) = 14 +/- 2.3 nmol/hr/mg; mean +/- SD; N = 3 different livers) and human B-lymphoblastoid cell microsomes containing cDNA-expressed CYP1A2 (K(m) = 46 microM; V(max) = 55 nmol/hr/nmol CYP), PODase activity conformed to monophasic Michaelis-Menten kinetics. Furthermore, PODase activity in a panel of microsomes prepared from a series of human livers was significantly correlated (r = 0.91; p < 0.001; N = 11) with CYP1A2-selective 7-ethoxyresorufin O-deethylase activity, and was markedly inhibited (> or = 92%) by furafylline (FURA, IC50 = 0.4 microM) and 7,8-benzoflavone (ANF, IC50 = 0.1 microM), two well known CYP1A2 inhibitors. Inhibitors selective for other forms of CYP (e.g. CYP3A, CYP2C, CYP2D6, CYP2E1) elicited a marginal effect (< or = 17% inhibition) at relatively high concentrations (> or = 10.K(i)). It is concluded that the inhibition of human liver microsomal CYP1A2 activity can be readily determined by using a charcoal-based radiometric method employing [O-ethyl 14C]phenacetin as substrate.     

A chemoenzymatic synthesis of UDP-(2-deoxy-2-fluoro)-galactose and evaluation of its interaction with galactosyltransferase

The left internal mammary artery-to-the left pulmonary artery shunt was created in a 16-year-old boy with single ventricle, severe pulmonary stenosis palliated by Glenn shunt at the age of two. Four years follow-up angiogram demonstrated a significant increase of the diameter of the left internal mammary artery from 4 to 7 mm. The internal mammary artery is a good alternative conduit for a systemic-to-pulmonary artery shunt for a cyanotic heart disease because of its growth potential.     

Mutation of the htrB gene in a virulent Salmonella typhimurium strain by intergeneric transduction: strain construction and phenotypic characterization

The htrB gene product of Haemophilus influenzae contributes to the toxicity of the lipooligosaccharide. The htrB gene encodes a 2-keto-3-deoxyoctulosonic acid-dependent acyltransferase which is responsible for myristic acid substitutions at the hydroxy moiety of lipid A beta-hydroxymyristic acid. Mass spectroscopic analysis has demonstrated that lipid A from an H. influenzae htrB mutant is predominantly tetraacyl and similar in structure to lipid IV(A), which has been shown to be nontoxic in animal models. We sought to construct a Salmonella typhimurium htrB mutant in order to investigate the contribution of htrB to virulence in a well-defined murine typhoid model of animal pathogenesis. To this end, an r- m+ galE mutS recD strain of S. typhimurium was constructed (MGS-7) and used in inter- and intrastrain transduction experiments with both coliphage P1 and Salmonella phage P22. The Escherichia coli htrB gene containing a mini-Tn10 insertion was transduced from E. coli MLK217 into S. typhimurium MGS-7 via phage P1 and subsequently via phage P22 into the virulent Salmonella strain SL1344. All S. typhimurium transductants showed phenotypes similar to those described for the E. coli htrB mutant. Mass spectrometric analysis of the crude lipid A fraction from the lipopolysaccharide of the S. typhimurium htrB mutant strain showed that for the dominant hexaacyl form, a lauric acid moiety was lost at one position on the lipid A and a palmitic acid moiety was added at another position; for the less abundant heptaacyl species, the lauric acid was replaced with palmitoleic acid.     

Global phylogeography of the ridley sea turtles (Lepidochelys spp.) as inferred from mitochondrial DNA sequences

BACKGROUND: The cardiovascular applications of magnetic resonance (MR) techniques in coronary artery disease have increased considerably in recent years. Technical advantages of MR imaging are the excellent spatial resolution, the characterization of myocardial tissue, and the potential for three-dimensional imaging. These characteristics allow the accurate assessment of left ventricular mass and volume, the differentiation of infarcted from normal tissue, and the determination of systolic wall thickening and regional wall motion abnormalities. METHODS: In addition to the conventionally used spin-echo and cine-echo techniques, newer techniques such as myocardial tagging, ultrafast MR imaging and MR coronary angiography have been developed. These newer techniques allow a more accurate assessment of ventricular function (tagging), myocardial perfusion (ultrafast imaging), and evaluation of stenosis severity (MR coronary angiography). Particularly early detection and flow assessment of stenosed coronary arteries and bypasses by MR angiography would constitute a major breakthrough in cardiovascular MR imaging. Apart from the MR imaging techniques, cardiac metabolism may be well assessed using MR spectroscopy. This provides unique information on the metabolic behaviour of the myocardium under conditions stress-induced ischemia. However, the definite niche of cardiac MR spectroscopy has still to be settled. CONCLUSION: Currently, MR techniques allow the evaluation of anatomy and function (accepted use), perfusion and viability (development phase), and coronary angiography (experimental phase). A particular strength of MR imaging is that one single MR test may encompass cardiac anatomy, perfusion, function, metabolism and coronary angiography. The replacement of multiple diagnostic tests with one MR test may have major effects on cardiovascular healthcare economics and would outweight the cost inherent to the MR angiography procedure.     

Association and colocalization of the Kvbeta1 and Kvbeta2 beta-subunits with Kv1 alpha-subunits in mammalian brain K+ channel complexes

The differential expression and association of cytoplasmic beta-subunits with pore-forming alpha-subunits may contribute significantly to the complexity and heterogeneity of voltage-gated K+ channels in excitable cells. Here we examined the association and colocalization of two mammalian beta-subunits, Kvbeta1 and Kvbeta2, with the K+ channel alpha-subunits Kv1.1, Kv1.2, Kv1.4, Kv1.6, and Kv2.1 in adult rat brain. Reciprocal coimmunoprecipitation experiments using subunit-specific antibodies indicated that Kvbeta1 and Kvbeta2 associate with all the Kv1 alpha-subunits examined, and with each other, but not with Kv2.1. A much larger portion of the total brain pool of Kv1-containing channel complexes was found associated with Kvbeta2 than with Kvbeta1. Single- and multiple-label immunohistochemical staining indicated that Kvbeta1 codistributes extensively with Kv1.1 and Kv1.4 in cortical interneurons, in the hippocampal perforant path and mossy fiber pathways, and in the globus pallidus and substantia nigra. Kvbeta2 codistributes extensively with Kv1.1 and Kv1.2 in all brain regions examined and was strikingly colocalized with these alpha-subunits in the juxtaparanodal region of nodes of Ranvier as well as in the axons and terminals of cerebellar basket cells. Taken together, these data provide a direct demonstration that Kvbeta1 and Kvbeta2 associate and colocalize with Kv1 alpha-subunits in native tissues and provide a biochemical and neuroanatomical basis for the differential contribution of Kv1 alpha- and beta-subunits to electrophysiologically diverse neuronal K+ currents.