Serum Cortisol level in children with catecholamine dependent shock: A Prospective Observational study

BACKGROUND: Adrenal glucocorticoid cortisol maintains the cardiovascular function, decreases the catabolism and stabilizes the alveolar capillary membrane during inflammatory stress period. AIM OF THE STUDY: To determine the prevalence of adrenal insufficiency by measuring serum cortisol level in children with catecholamine dependent septic shock. METHOD: 49 children admitted with catecholamine dependant septic shock satisfying inclusion criteria recruited in to the study. Random serum cortisol was measured and correlated with various prognostic parameters like duration of inotropic and ventilator support, PICU and hospital stay and mortality. RESULT: The prevalence of adrenal insufficiency (< 18μgm/dl) was 41%. Duration of inotropic support (Median of 3 vs 2 days; P= 0.04), ventilator days (Median of 2.5 vs 1 day; P = 0.001) and proportionately the PICU stays (Median of 5 vs 4 days; P = 0.03) were significantly prolonged in the children with low cortisol when compared to children with normal cortisol level. Whereas the total duration of hospital stay (Median days of 10 vs 7; P=0.07) and the mortality (7 children in each group 35% vs 24%; p=0.304) were comparable between the two groups. CONCLUSION: we concluded that the low serum cortisol was a common finding among children suffering catecholamine dependent septic shock and it was positively correlated with prolonged hemodynamic, respiratory support and ICU care. We require further study to delineate the incidence of absolute and relative adrenal insufficiency by doing a stimulation test and also require controlled randomized trials to analyse the benefits of steroid supplementation on morbidity and mortality of these children

Effect of PVA doping on flux pinning in Bulk MgB2

The synthesis and characterization of PVA (Poly Vinyl Acetate) doped bulk MgB2 superconductor is reported here. PVA is used as a Carbon source. PVA doping effects made two distinguishable contributions: first enhancement of Jc field performance and second an increase in Hc2 value, both because of carbon incorporation into MgB2 crystal lattice. The susceptibility measurement reveals that Tc decreased from 37 to 36 K. Lattice parameter a decreased from 3.085 A to 3.081 A due to the partial substitution of Carbon at Boron site. PVA doped sample exhibited the Jc values greater than 10^5 A/cm2 at 5 & 10 K at low fields; which is almost 3 times higher than the pure one, while at high fields the Jc is increased by an order of magnitude in comparison to pure MgB2. From R(T)H measurements we found higher Tc values under magnetic field for doped sample; indicating an increase in Hc2. Also the magnetization measurements exhibited a significant enhancement in Hirr value. The improved performance of PVA doped MgB2 can be attributed to the substitution of carbon at boron site in parent MgB2 and the resulting impact on the carrier density and impurity scattering. The improved flux pinning behavior could easily be seen from reduced flux pinning force plots.Comment: 14 Pages of Text + Figs. To appear in Physica

Born Effective Charges and Infrared Response of LiBC

Calculations of the zone center optical mode frequencies (including LO-TO splitting), Born effective charges Z$^*_{\alpha\alpha}$ for each atom, dielectric constants $\epsilon_{0}$ and $\epsilon_{\infty}$, and the dielectric response in the infrared, using density functional linear response theory, are reported. Calculated Raman modes are in excellent agreement with experimental values (170 cm$^{-1}$ and 1170 cm$^{-1}$), while it will require better experimental data to clarify the infrared active mode frequencies. The Born effective charges Z$^*_{\alpha \alpha}$ (i) have surprisingly different values for B and C, and (ii) show considerable anisotropy. Relationships between the effective charges and LO-TO splitting are discussed, and the predicted reflectivity in the range 0 -- 1400 cm$^{-1}$ is presented. These results hold possible implications for Li removal in LiBC, and C substition for B in MgB$_2$.Comment: 6 pages, 3 figure

Self-Compassion and Depressive Symptoms as Determinants of Sensitive Parenting: Associations with Sociodemographic Characteristics in a Sample of Mothers and Toddlers

Parenting that is sensitive and responsive to children’s needs has been shown to support children’s optimal growth and development in many cultural contexts. Numerous studies suggest that self-compassion is positively related to sensitive parenting. Despite growing research interest linking self-compassion to responsive parenting, there are considerable gaps in the literature. The current study examined the associations between self-compassion, depressive symptoms, socioeconomic status, and sensitive parenting. Data was obtained from a cohort study of 300 families in central Ohio enrolled when children were a mean (SD) calendar age of 18.2 (0.7) months. Children of all gestational ages at birth are included, and 37% were born preterm (<37 weeks’ gestation). Observational protocols were used to determine maternal sensitivity in a semi-structured play setting. Self-compassion was assessed with the Self-Compassion Scale when children were 24 months old. Self-compassion was not associated with sociodemographic characteristics including maternal education, household income, child sex and gestational age. In unadjusted regression models, depressive symptoms were related to sensitive parenting (B = −0.036, SE = 0.016, p = 0.03), but self-compassion was not a statistically significant predictor (p = 0.35) of sensitivity, and neither self-compassion nor depressive symptoms were statistically significant predictors of sensitive parenting after adjustment for covariates. Considerations for future studies are discussed

Quaternionic Salkowski Curves and Quaternionic Similar Curves

In this paper, we give the definitions and characterizations of quaternionic Salkowski, quaternionic anti-Salkowski and quaternionic similar curves in the Euclidean spaces E^3 and E^4. We obtain relationships between these curves and some special quaternionic curves such as quaternionic slant helices and quaternionic B2-slant helices.Comment: 17 page

A novel bacteriophage Tail-Associated Muralytic Enzyme (TAME) from Phage K and its development into a potent antistaphylococcal protein

<p>Abstract</p> <p>Background</p> <p><it>Staphylococcus aureus </it>is a major cause of nosocomial and community-acquired infections. However, the rapid emergence of antibiotic resistance limits the choice of therapeutic options for treating infections caused by this organism. Muralytic enzymes from bacteriophages have recently gained attention for their potential as antibacterial agents against antibiotic-resistant gram-positive organisms. Phage K is a polyvalent virulent phage of the <it>Myoviridae </it>family that is active against many <it>Staphylococcus </it>species.</p> <p>Results</p> <p>We identified a phage K gene, designated <it>orf</it>56, as encoding the phage tail-associated muralytic enzyme (TAME). The gene product (ORF56) contains a C-terminal domain corresponding to cysteine, histidine-dependent amidohydrolase/peptidase (CHAP), which demonstrated muralytic activity on a staphylococcal cell wall substrate and was lethal to <it>S. aureus </it>cells. We constructed N-terminal truncated forms of ORF56 and arrived at a 16-kDa protein (Lys16) that retained antistaphylococcal activity. We then generated a chimeric gene construct encoding Lys16 and a staphylococcal cell wall-binding SH3b domain. This chimeric protein (P128) showed potent antistaphylococcal activity on global clinical isolates of <it>S. aureus </it>including methicillin-resistant strains. In addition, P128 was effective in decolonizing rat nares of <it>S. aureus </it>USA300 in an experimental model.</p> <p>Conclusions</p> <p>We identified a phage K gene that encodes a protein associated with the phage tail structure. The muralytic activity of the phage K TAME was localized to the C-terminal CHAP domain. This potent antistaphylococcal TAME was combined with an efficient <it>Staphylococcus</it>-specific cell-wall targeting domain SH3b, resulting in the chimeric protein P128. This protein shows bactericidal activity against globally prevalent antibiotic resistant clinical isolates of <it>S. aureus </it>and against the genus <it>Staphylococcus </it>in general. <it>In vivo</it>, P128 was efficacious against methicillin-resistant <it>S. aureus </it>in a rat nasal colonization model.</p

Study of various congenital anomalies in fetal and neonatal autopsy

Background: The study of dead is to save the livings. The growing awareness that still births and infant mortalities are unable to reduction has led to a wide spread desire for more information regarding the cause of these deaths. Congenital malformations have become important cause of fetal and neonatal (perinatal) mortality in developed countries and would very soon be increasingly important determinants of fetal and neonatal mortality in developing countries like India. In spite of antenatal diagnostic modality still the fetal autopsy plays the vital role in the conformation as well as identification of congenital anomalies and also for the counseling of the parents, to prevent the fetal congenital anomalies in further pregnancies. This study was undertaken with the purpose of finding out cause of death during the perinatal period at government maternity hospital and pediatric department S.V.R.R.G.G.H. & S.V. medical college Tirupati, and to study the clinical and pathological findings (Gross & microscopic) in fetal and neonatal death.Methods: The present study of congenital anomalies in fetal and neonatal deaths was done at S.V. medical college, Tirupati, over a time period of 2 years from September 2008 to 2010 August. Consent for autopsy in requested compassionately, respectfully and fully informed. The present study included dead fetus and neonates with gestational age above 20 weeks of intra uterine life and within 7 days of post natal life. All fetuses of gestational age <20 weeks and all neonates above 7 days of age were excluded from the study. The study also obtained clearance from the ethical committee of the institution. Autopsy was performed by standard technique adopted by Edith L. Potter. External and internal findings followed by histopathological examination, and autopsy findings were compared with available ultrasound findings.Results: A total of 46 Autopsies performed, 40 (87%) were fetal deaths, 6 (13%) were early neonatal deaths. In a total of 46 fetuses, there were 13 male and 33 female babies. On external examination of 46 fetal and Neonatal (perinatal) deaths, 8 (17.39%) babies showed congenital malformation. On internal examination of the 46 fetal and Neonatal (perinatal) deaths, 4 babies showed internal congenital anomalies. A total of 46 anatomical and histopathologic examinations were done among fetal and neonatal (perinatal) deaths. Out of 13 autopsies on male babies, 2 had congenital malformation and 33 autopsies on female babies, 7 had congenital malformations. Congenital anomalies were commonest in the birth weight group of 1000-1500 grams accounting for 9 cases. Malformations of central nervous system (33.33%) were most common followed by musculoskeletal system (16.66%), genitourinary and respiratory system (8.33%) respectively.Conclusion: Most number of perinatal deaths occurred in low birth weight and preterm babies. Study of malformations greatly helpful in genetic counseling and prenatal diagnosis in successive pregnancies

Aberrant activation of TCL1A promotes stem cell expansion in clonal haematopoiesis

Mutations in a diverse set of driver genes increase the fitness of haematopoietic stem cells (HSCs), leading to clonal haematopoiesis1. These lesions are precursors for blood cancers2,3,4,5,6, but the basis of their fitness advantage remains largely unknown, partly owing to a paucity of large cohorts in which the clonal expansion rate has been assessed by longitudinal sampling. Here, to circumvent this limitation, we developed a method to infer the expansion rate from data from a single time point. We applied this method to 5,071 people with clonal haematopoiesis. A genome-wide association study revealed that a common inherited polymorphism in the TCL1A promoter was associated with a slower expansion rate in clonal haematopoiesis overall, but the effect varied by driver gene. Those carrying this protective allele exhibited markedly reduced growth rates or prevalence of clones with driver mutations in TET2, ASXL1, SF3B1 and SRSF2, but this effect was not seen in clones with driver mutations in DNMT3A. TCL1A was not expressed in normal or DNMT3A-mutated HSCs, but the introduction of mutations in TET2 or ASXL1 led to the expression of TCL1A protein and the expansion of HSCs in vitro. The protective allele restricted TCL1A expression and expansion of mutant HSCs, as did experimental knockdown of TCL1A expression. Forced expression of TCL1A promoted the expansion of human HSCs in vitro and mouse HSCs in vivo. Our results indicate that the fitness advantage of several commonly mutated driver genes in clonal haematopoiesis may be mediated by TCL1A activation