Assessing Community Based Improved Maternal Neonatal Child Survival (IMNCS) Program in Rural Bangladesh

Objectives

A community based approach before, during and after child birth has been proven effective address the burden of maternal, neonatal and child morbidity and mortality in the low and middle income countries. We aimed to examine the overall change in maternal and newborn health outcomes due the “Improved Maternal Newborn and Child Survival” (IMNCS) project, which was implemented by BRAC in rural communities of Bangladesh.

Methods

The intervention was implemented in four districts for duration of 5-years, while two districts served as comparison areas. The intervention was delivered by community health workers who were trained on essential maternal, neonatal and child health care services. A baseline survey was conducted in 2008 among 7, 200 women with pregnancy outcome in last year or having a currently alive child of 12–59 months. A follow-up survey was administered in 2012–13 among 4, 800 women of similar characteristics in the same villages.

Findings

We observed significant improvements in maternal and essential newborn care in intervention areas over time, especially in health care seeking behaviors. The proportion of births taking place at home declined in the intervention districts from 84.3% at baseline to 71.2% at end line (P<0.001). Proportion of deliveries with skilled attendant was higher in intervention districts (28%) compared to comparison districts (27.4%). The number of deliveries was almost doubled at public sector facility comparing with baseline (P<0.001). Significant improvement was also observed in healthy cord care practice, delayed bathing of the new-born and reduction of infant mortality in intervention districts compared to that of comparison districts.

Conclusions

This study demonstrates that community-based efforts offer encouraging evidence and value for combining maternal, neonatal and child health care package. This approach might be considered at larger scale in similar settings with limited resources.     

Alterations in Ca2+ homeostasis in rat erythrocytes with atrazine treatment: positive modulation by vitamin E

Tubulin polymerization promoting protein 3 (TPPP3), a member of the TPPP family, can induce tubulin polymerization and microtubule bundling. Previously, it has been shown that TPPP3 plays an important role in cell proliferation. Depletion of TPPP3 by microRNA-based RNA interference (RNAi) inhibits cell growth, arrests cell cycles, and causes mitotic abnormalities in HeLa cells. In the present study, we knocked down TPPP3 in Lewis lung carcinoma (LLC) cells with the same RNAi construct, and observed a retarded tumor cell growth in vitro. Furthermore, C57BL/6 mice that received subcutaneously injected LLC cells in which TPPP3 was knocked down showed a pronounced reduction in tumor progression. The migration/invasion activity of TPPP3-knockdown LLC cells was significantly suppressed in a transwell chamber migration assay. When these cells were injected into the tail veins of C57BL/6 mice, they exhibited milder lung metastasis compared with control tumor cells. Taken together, these findings suggested that the TPPP3 gene played an important role in tumorigenesis and metastasis, and it could potentially become a novel target for cancer therapy.     

Genetic characterization of mutants resistant to the antiauxin p-chlorophenoxyisobutyric acid reveals that AAR3, a gene encoding a DCN1-like protein, regulates responses to the synthetic auxin 2,4-dichlorophenoxyacetic acid in Arabidopsis roots

To isolate novel auxin-responsive mutants in Arabidopsis (Arabidopsis thaliana), we screened mutants for root growth resistance to a putative antiauxin, p-chlorophenoxyisobutyric acid (PCIB), which inhibits auxin action by interfering the upstream auxin-signaling events. Eleven PCIB-resistant mutants were obtained. Genetic mapping indicates that the mutations are located in at least five independent loci, including two known auxin-related loci, TRANSPORT INHIBITOR RESPONSE1 and Arabidopsis CULLIN1. antiauxin-resistant mutants (aars) aar3-1, aar4, and aar5 were also resistant to 2,4-dichlorophenoxyacetic acid as shown by a root growth assay. Positional cloning of aar3-1 revealed that the AAR3 gene encodes a protein with a domain of unknown function (DUF298), which has not previously been implicated in auxin signaling. The protein has a putative nuclear localization signal and shares homology with the DEFECTIVE IN CULLIN NEDDYLATION-1 protein through the DUF298 domain. The results also indicate that PCIB can facilitate the identification of factors involved in auxin or auxin-related signaling.     

Modularized study of human calcium signalling pathway

Signalling pathways are complex biochemical networks responsible for regulation of numerous cellular functions. These networks function by serial and successive interactions among a large number of vital biomolecules and chemical compounds. For deciphering and analysing the underlying mechanism of such networks,a modularized study is quite helpful. Here we propose an algorithm for modularization of calcium signalling pathway of H. sapiens .The idea that "a node whose function is dependent on maximum number of other nodes tends to be the center of a sub network" is used to divide a large signalling network into smaller sub networks. Inclusion of node(s) into sub networks(s) is dependent on the outdegree of the node(s). Here outdegree of a node refers to the number of relations of the considered node lying outside the constructed sub network. Node(s) having more than c relations lying outside the expanding sub network have to be excluded from it. Here c is a specified variable based on user preference, which is finally fixed during adjustments of created sub networks, so that certain biological significance can be conferred on them.     

Supramolecular networks of dinuclear copper(II): Synthesis, crystal structure and magnetic study

The complexes [Cu₂(ox)(phen)₂(H₂O)₂](NO₃)₂ (1), [Cu₂(sq)(pmdien)₂(H₂O)₂](ClO₄)₂ (2) and {[Cu₃(pdc)₃(4,4′-bipy)_1.5(H₂O)_2.25] · 2.5(H₂O)}_n (3) [phen = 1,10-phenanthroline; pmdien = N,N,N′,N′,N″-pentamethyldiethylenetriamine; 4,4′-bipy = 4,4′-bipyridine; ox = oxalate dianion; sq = squarate dianion and pdc = pyridine 2,6-dicarboxylate] have been synthesized and characterized by X-ray single crystal structure determination, low temperature magnetic measurement and thermal study. Structure determination reveals that 1 and 2 are dinuclear copper(II) complexes bridged by oxalate and squarate dianions, respectively, while 3 is a hexanuclear species formed by three Cu(pdc)(H₂O)-(4,4′-bipy)-Cu(pdc)(H₂O) fragments, connected through long Cu-O(pdc) bonds in a centrosymmetric arrangement. In complex 1 H-bonds occurring between the coordinated water molecules and lattice nitrate anions result in eight-membered ring clusters with the concomitant formation of 1D supramolecular chain. The adjacent chains undergo π-π stacking forming a 2D architecture. In the crystal of 3 an extensive H-bonding scheme gives rise to a 3D supramolecular network. Low temperature magnetic study shows a strong antiferromagnetic coupling in 1 (J = −288 ± 2 cm⁻¹, g = 2.21 ± 0.01, R = 1.2 × 10⁻⁶); and a very weak interaction in 2 and 3, the best-fit parameters being: J = −0.21 cm⁻¹, g = 2.12 ± 0.01, R = 1.1 × 10⁻⁶ (2) and J = −1.34 cm⁻¹ ± 0.1, g = 2.14 ± 0.01, R = 1.2 × 10⁻⁶ (3) (R defines as .     

Human ribosomal protein L13a is dispensable for canonical ribosome function but indispensable for efficient rRNA methylation

Previously, we demonstrated that treatment of monocytic cells with IFN-gamma causes release of ribosomal protein L13a from the 60S ribosome and subsequent translational silencing of Ceruloplasmin (Cp) mRNA. Here, evidence using cultured cells demonstrates that Cp mRNA silencing is dependent on L13a and that L13a-deficient ribosomes are competent for global translational activity. Human monocytic U937 cells were stably transfected with two different shRNA sequences for L13a and clonally selected for more than 98% abrogation of total L13a expression. Metabolic labeling of these cells showed rescue of Cp translation from the IFN-gamma mediated translational silencing activity. Depletion of L13a caused significant reduction of methylation of ribosomal RNA and of cap-independent translation mediated by Internal Ribosome Entry Site (IRES) elements derived from p27, p53, and SNAT2 mRNAs. However, no significant differences in the ribosomal RNA processing, polysome formation, global translational activity, translational fidelity, and cell proliferation were observed between L13a-deficient and wild-type control cells. These results support the notion that ribosome can serve as a depot for releasable translation-regulatory factors unrelated to its basal polypeptide synthetic function. Unlike mammalian cells, the L13a homolog in yeast is indispensable for growth. Thus, L13a may have evolved from an essential ribosomal protein in lower eukaryotes to having a role as a dispensable extra-ribosomal function in higher eukaryotes.