An alternative technique for intracardiac exposure during transatrial repair of tetralogy of fallot

The commonly used technique to facilitate intracardiac exposure during transatrial repair of tetralogy of fallot involves considerable retraction of the tricuspid valve using retractors. We describe an alternative surgical technique in which it is possible to dispense away with the retractors. The advantages of such a technique are discussed.     

Preliminary noise reduction efforts in a medical intensive care unit

Noise is a significant contributor to sleep disruption in the intensive care unit (ICU) that may result in increased patient morbidity such as delirium and prolonged length of stay in ICU. We conducted a pre-post intervention study in a 24-bed tertiary care academic medical ICU to reduce the mean noise levels. Baseline dosimeter recordings of ICU noise levels demonstrated a mean noise level of 54.2 A-weighted decibels (dBA) and peak noise levels of 109.9 dBA, well above the Environmental Protection Agency’s recommended levels. There were 1735 episodes of “defects” (maximum noise levels > 60 dBA). Following implementation of multipronged interventions, although the mean noise levels did not change significantly between pre- and post-intervention (54.2 vs 53.8 dBA; p = 0.96), there was a significant reduction in the number of “defects” post-intervention (1735 vs 1289, p ≤ 0.000), and the providers felt that the patients were sleeping longer in the ICU post-intervention.     

Center of pressure and the projection of the time-course of sitting skill acquisition

A normal time-course for the acquisition of sitting is essential. A delay in sitting may affect other developmental milestones, resulting in deficiencies in overall skill. Therefore, our aim was to identify variables whose measures at the very beginning of sitting would allow for the projection of the evolution of the sitting skill. Center of pressure data were collected from the postural sway of twenty-six typically developing infants while sitting on a force platform with a beginning ability to sit upright. Spatial, temporal and frequency variables of postural sway were obtained from both the medial/lateral and anterior/posterior directions of sway. Discriminant function analysis was conducted to identify potential predictors of the duration between onset and fully independent sitting. Gender (p = 0.025), median frequency (p = 0.006), and correlation dimension (p = 0.002) were identified to be predictive of grouping with 73.1% correct classification of the participating infants into short, mid, and long delay groups. In conclusion, measures taken at the earliest stage of sitting may allow the projection of the time-course to achieve independent sitting for typical infants. This approach may be useful for monitoring typical development.     

Cysteamine-induced depletion of brain somatostatin is associated with up-regulation of cerebrocortical somatostatin receptors

Cysteamine (CSH) administered as a single sc injection to rats produced rapid depletion of cerebrocortical Somatostatin-14 like immunoreactivity (S-14 LI) with a significant 48% reduction occurring within 5 min and maximum (72%) decrease at 4 h. The depletion of S-14 LI was associated with a 1.7 fold increase in Bmax of the cerebrocortical S-14 receptors 5 min after CSH administration and a concomitant but slower increase in the affinity of these receptors [dissociation constant (Kd) being 1.8- and 1.6-fold lower than the control at 30 and 60 min, respectively, post CSH]. Incubation of intact synaptosomes with 1 mM CSH at 37 C in vitro for 60 min also caused a rapid depletion of S-14 LI, but in contrast to the in vivo data, there was no change in the Bmax or Kd of the S-14 receptors for up to 30 min beyond which time a 2.8-fold decrease in the affinity of S-14 receptors was observed. Higher concentrations of CSH (greater than or equal to 10 mM) added during the incubation of synaptosomes in vitro completely abolished the specific binding of these receptors. The pituitary S-14 receptors were studied 30 min after CSH administration and unlike the cerebrocortical S-14 receptors at this time did not exhibit any change in Bmax or affinity. When added at the time of the binding assay CSH (1 mM) was without a direct effect on cerebrocortical as well as pituitary membrane S-14 receptors. Furthermore, addition of CSH at the time of binding assay did not destroy the integrity of [125I-Tyr11]S-14. It is concluded that administration of CSH to rats in vivo depletes brain S-14 LI and up-regulates synaptosomal S-14 receptors. Exposure of synaptosomes to CSH in vitro for 30 min also depletes S-14 LI but has no effect on S-14 receptors suggesting that S-14 receptor regulation by S-14 is an in vivo phenomenon or requires the intact cell. CSH has a direct inhibitory effect on S-14 receptor binding after prolonged in vitro incubation. Pituitary S-14 receptors unlike those in the brain are unaffected by S-14 LI depletion at least acutely.     

Mechanisms which mediate the antiapoptotic effects of angiopoietin-1 on endothelial cells

The main objective of this study was to identify molecular mechanisms through which angiopoietin-1 (Ang-1), a ligand for Tie-2 receptors, influences endothelial cell apoptosis. Human umbilical vein endothelial cells were cultured in a medium enriched with 2% fetal bovine serum (FBS) and growth supplements. Apoptosis was induced over 24 h by reducing FBS to 0.1%. Activation of caspase-9, -8, -7, and -3 and the expression of Bcl-2 family proteins, inhibitors of apoptosis (IAPs), cytochrome c, as well as Smac proteins were evaluated with immunoblotting. Ang-1 clearly attenuated serum deprivation-evoked apoptosis, an effect which required Tie-2 receptor activation. Activation of caspase-9, -7, and -3, but not caspase-8, was inhibited by Ang-1. The inhibitory effects of Ang-1 on apoptosis and caspase activation were reversed by a PI-3 kinase inhibitor (wortmannin). Ang-1 exposure upregulated the expression of Survivin but not XIAP (members of IAPs), reduced the cystosolic levels of Smac, but not that of cytochrome c, and had no effect on the expression of Bcl-2 family proteins. This is the first study to report on the mitochondrial mechanisms through which Ang-1 inhibits apoptosis and to investigate the role of the newly discovered Smac. We conclude that Ang-1 inhibits endothelial cell apoptosis through several pathways, which include PI-3 kinase/AKT activation, inhibition of Smac release from the mitochondria, and upregulation of Survivin protein.     

Evidence for the presence of glucagon-like immunoreactivity (GLI) in the pancreas.

Glucagon-like immunoreactivity (GLI), which can be separated from glucagon by isoelectric focusing, has been detected in partially purified canine pancreatic extracts. Like gastrointestinal GLI, this insular GLI reacts with crossreacting antiserum 78J but not with glucagon "specific" antiserum 30K and has an isoelectric point (pl) of 9.5, whereas canine pancreatic glucagon has a pl of 6.25. When combined with glucagon, the GLI-glucagon mixture gives 48J assay values between GLI and this crossreacting antiglucagon serum and thus conceals it in glucagon-containing extracts.     

Correlation between peripheral arterial disease and coronary artery disease using ankle brachial index-a study in Indian population

ObjectiveTo study the prevalence of peripheral arterial disease (PAD) of the lower limbs in a high-risk population and its correlation with coronary artery disease (CAD), using the ankle brachial index (ABI).MethodsThe present study was conducted in randomly selected indoor patients >45 years of age with one or more risk factors for PAD admitted in the cardiology and medicine wards in a tertiary care institute.ResultsBased on ABI <0.9, PAD was diagnosed in 32 of the 182 (18%) patients. Coronary artery disease was present in 15 cases of PAD which was statistically significant.ConclusionThere is a definite and strong correlation between PAD and CAD. Correct diagnosis and supervision of patients with PAD is important for preventing the local progression of the disease and effective secondary prevention of future coronary and cerebrovascular events.     

Cell of origin strongly influences genetic selection in a mouse model of T-ALL

Identifying the normal cell from which a tumor originates is crucial to understanding the etiology of that cancer. However, retrospective identification of the cell of origin in cancer is challenging because of the accumulation of genetic and epigenetic changes in tumor cells. The biologic state of the cell of origin likely influences the genetic events that drive transformation. We directly tested this hypothesis by performing a Sleeping Beauty transposon mutagenesis screen in which common insertion sites were identified in tumors that were produced by mutagenesis of cells at varying time points throughout the T lineage. Mutation and gene expression data derived from these tumors were then compared with data obtained from a panel of 84 human T-cell acute lymphoblastic leukemia samples, including copy number alterations and gene expression profiles. This revealed that altering the cell of origin produces tumors that model distinct subtypes of human T-cell acute lymphoblastic leukemia, suggesting that even subtle changes in the cell of origin dramatically affect genetic selection in tumors. These findings have broad implications for the genetic analysis of human cancers as well as the production of mouse models of cancer.