Birth Preparedness and Complication Readiness among Pregnant Women in Duguna Fango District,Wolayta Zone,Ethiopia

Background

Birth Preparedness and Complication Readiness is a strategy to promote the timely use of skilled maternal and neonatal care, especially during childbirth, based on the theory that preparing for childbirth and being ready for complications reduces delays in obtaining this care.

Objective

This study was conducted to assess birth preparedness and complication readiness and its associated factors among pregnant woman in Duguna Fango District in Wolayta Zone, South Ethiopia.

Methods

A community based cross-sectional study was conducted in 2013, on a sample of 578 pregnant women. Data were collected using pre-tested and structured questionnaire. The collected data were analyzed by SPSS for windows version 16.0. The women were asked whether they followed the desired five steps while pregnant: identified a trained birth attendant, identified a health facility, arranged for transport, identified blood donor and saved money for emergency. Taking at least three steps was considered being well-prepared.

Results

Among 578 pregnant women only one tenth (10.7%) of pregnant women identified skilled provider. Only 103 (18.1%) arranged transportation to health facility. Two hundred forty eight (43.6%) identified health facility for delivery and/or for obstetric emergencies. more than half (54.1%) of families saved money for incurred costs of delivery and emergency if needed. only few 17(3%) identified potential blood donor in case of emergency. Two hundred sixty four (46.4%) of the respondents reported that they intended to deliver at home, and more than half (53.6) planned to deliver at health facilities. Overall less than one fifth 18.3% of pregnant women were well prepared. The adjusted multivariate model showed that significant predictors for being well-prepared were maternal availing of antenatal services (AOR = 2.95, 95% CI: 1.62–5.37), being pregnant for the first time (AOR = 3.37, 95% CI: 1.45–7.82), having knowledge of at least two danger signs during pregnancy (AOR = 2.81, 95% CI: 1.69–4.67) and history of past obstetric complication (AOR = 2.98, 95% CI: 1.35–6.58).

Conclusion

Birth preparedness practice in the study area was found to be low. Information, Education and Communication (IEC) on birth preparedness and complication readiness for young people should start early adolescence. The government officials and partners that are working in areas of maternal health should come up with strategies to improve birth preparedness at individual and community level.     

Functional LCAT deficiency in human apolipoprotein A-I transgenic, SR-BI knockout mice

Reduction of plasma LCAT activity has been observed in several conditions in which the size of HDL particles is increased; however, the mechanism of this reduction remains elusive. We investigated the plasma activity, mass, and in vivo catabolism of LCAT and its association with HDL particles in human apolipoprotein A-I transgenic, scavenger receptor class B type I knockout (hA-ITg SR-BI-/-) mice. Compared with hA-ITg mice, hA-ITg SR-BI-/- mice had a 4-fold higher total plasma cholesterol concentration, which occurred predominantly in 13-18 nm diameter HDL particles, a significant reduction in plasma esterified cholesterol-total cholesterol (EC/TC) ratio, and significantly lower plasma LCAT activity, suggesting a decrease in LCAT protein. However, LCAT protein in plasma, hepatic mRNA for LCAT, and in vivo turnover of 35S-radiolabeled LCAT were similar in both genotypes of mice. HDL from hA-ITg SR-BI-/- mice was enriched in sphingomyelin (SM), relative to phosphatidylcholine, and had less associated [35S]LCAT radiolabel and endogenous LCAT activity compared with HDL from hA-ITg mice. We conclude that the decreased EC/TC ratio in the plasma of hA-ITg SR-BI-/- mice is attributed to a reduction in LCAT reactivity with SM-enriched HDL particles.     

Revealing Neural Circuit Topography in Multi-Color

Neural circuits are organized into functional topographic maps. In order to visualize complex circuit architecture we developed an approach to reliably label the global patterning of multiple topographic projections. The cerebellum is an ideal model to study the orderly arrangement of neural circuits. For example, the compartmental organization of spinocerebellar mossy fibers has proven to be an indispensable system for studying mossy fiber patterning. We recently showed that wheat germ agglutinin (WGA) conjugated to Alexa 555 and 488 can be used for tracing spinocerebellar mossy fiber projections in developing and adult mice (Reeber et al. 2011). We found three major properties that make the WGA-Alexa tracers desirable tools for labeling neural projections. First, Alexa fluorophores are intense and their brightness allows for wholemount imaging directly after tracing. Second, WGA-Alexa tracers label the entire trajectory of developing and adult neural projections. Third, WGA-Alexa tracers are rapidly transported in both retrograde and anterograde directions. Here, we describe in detail how to prepare the tracers and other required tools, how to perform the surgery for spinocerebellar tracing and how best to image traced projections in three dimensions. In summary, we provide a step-by-step tracing protocol that will be useful for deciphering the organization and connectivity of functional maps not only in the cerebellum but also in the cortex, brainstem, and spinal cord.Download video file.^{(58M, mov)}     

C75 activates malonyl-CoA sensitive and insensitive components of the CPT system

Carnitine palmitoyltransferase I (CPT-I) and II (CPT-II) enzymes are components of the carnitine palmitoyltransferase shuttle system which allows entry of long-chain fatty acids into the mitochondrial matrix for subsequent oxidation. This system is tightly regulated by malonyl-CoA levels since this metabolite is a strong reversible inhibitor of the CPT-I enzyme. There are two distinct CPT-I isotypes (CPT-Ialpha and CPT-Ibeta), that exhibit different sensitivity to malonyl-CoA inhibition. Because of its ability to inhibit fatty acid synthase, C75 is able to increase malonyl-CoA intracellular levels. Paradoxically it also activates long-chain fatty acid oxidation. To identify the exact target of C75 within the CPT system, we expressed individually the different components of the system in the yeast Pichia pastoris. We show here that C75 acts on recombinant CPT-Ialpha, but also on the other CPT-I isotype (CPT-Ibeta) and the malonyl-CoA insensitive component of the CPT system, CPT-II.     

A novel role for ABCA1-generated large pre-�� migrating nascent HDL in the regulation of hepatic VLDL triglyceride secretion

In Tangier disease, absence of ATP binding cassette transporter A1 (ABCA1) results in reduced plasma HDL and elevated triglyceride (TG) levels. We hypothesized that hepatocyte ABCA1 regulates VLDL TG secretion through nascent HDL production. Silencing of ABCA1 expression in oleate-stimulated rat hepatoma cells resulted in: 1) decreased large nascent HDL (>10 nm diameter) and increased small nascent HDL (<10 nm) formation, 2) increased large buoyant VLDL1 particle secretion, and 3) decreased phosphatidylinositol-3 (PI3) kinase activation. Nascent HDL-containing conditioned medium from rat hepatoma cells or HEK293 cells transfected with ABCA1 was effective in increasing PI3 kinase activation and reducing VLDL TG secretion in ABCA1-silenced hepatoma cells. Addition of isolated large nascent HDL particles to ABCA1-silenced hepatoma cells inhibited VLDL TG secretion to a greater extent than small nascent HDL. Similarly, addition of recombinant HDL, but not human plasma HDL, was effective in attenuating TG secretion and increasing PI3 kinase activation in ABCA1-silenced cells. Collectively, these data suggest that large nascent HDL particles, assembled by hepatic ABCA1, generate a PI3 kinase-mediated autocrine signal that attenuates VLDL maturation and TG secretion. This pathway may explain the elevated plasma TG concentration that occurs in most Tangier subjects and may also account, in part, for the inverse relationship between plasma HDL and TG concentrations in individuals with compromised ABCA1 function.     

Ticks and tick-borne pathogens in livestock from nomadic herds in the Somali Region,Ethiopia

Between May 2006 and January 2007, blood samples and ticks were randomly collected from 220 nomadic animals from Filtu and Dollo Odo districts, Libaan zone, in the Somali Region of Ethiopia. Overall, 81.5% cattle, 98.2% camels, 53.4% goats and 61.1% sheep were infested by ixodid ticks. Collected ticks (n = 1,036) were identified as Rhipicephalus pulchellus (40.1%), R. pravus (25.8%), Amblyomma gemma (9.4%), Hyalomma rufipes (13.3%), H. truncatum (2.8%), H. impeltatum (1.2%) and H. dromedarii (0.5%); immature stages (6.1%) belonged to the genera Rhipicephalus and Amblyomma. Tick infestation burden was evaluated by the Tick Abundance Score method on 57 animals from Dollo Odo in August 2006, and it was significantly higher in cattle and camels than in small ruminants (p < 0.001). Reverse Line Blot Hybridisation was applied to detect Theileria, Babesia, Ehrlichia and Anaplasma spp. Five out of 50 blood samples from Filtu, four from cattle and, surprisingly, one from a camel, were positive for Theileria mutans and two from cattle for T. velifera. Adult ticks (n = 104) from both districts were tested and A. gemma from cattle were positive to T. velifera (1) and Ehrlichia ruminantium (5 samples). Positive E. ruminantium samples were also tested by PCR targeting pCS20 and 16S rRNA genes and submitted to DNA sequencing. The phylogenetic reconstruction of pCS20 fragment showed the presence of the Somali region sequences in the East-South African group. Our results are the first available on ticks and selected tick-borne diseases from the Somali region of Ethiopia and could be used as preliminary information for planning sustainable control strategies for tick and tick-borne pathogens in the study area and in neighbouring areas with similar socio-ecological features.     

Initial interaction of apoA-I with ABCA1 impacts in vivo metabolic fate of nascent HDL

We investigated the in vivo metabolic fate of pre-beta HDL particles in human apolipoprotein A-I transgenic (hA-I (Tg)) mice. Pre-beta HDL tracers were assembled by incubation of [(125)I]tyramine cellobiose-labeled apolipoprotein A-I (apoA-I) with HEK293 cells expressing ABCA1. Radiolabeled pre-beta HDLs of increasing size (pre-beta1, -2, -3, and -4 HDLs) were isolated by fast-protein liquid chromatography and injected into hA-I (Tg)-recipient mice, after which plasma decay, in vivo remodeling, and tissue uptake were monitored. Pre-beta2, -3, and -4 had similar plasma die-away rates, whereas pre-beta1 HDL was removed 7-fold more rapidly. Radiolabel recovered in liver and kidney 24 h after tracer injection suggested increased (P < 0.001) liver and decreased kidney catabolism as pre-beta HDL size increased. In plasma, pre-beta1 and -2 were rapidly (<5 min) remodeled into larger HDLs, whereas pre-beta3 and -4 were remodeled into smaller HDLs. Pre-beta HDLs were similarly remodeled in vitro with control or LCAT-immunodepleted plasma, but not when incubated with phospholipid transfer protein knockout plasma. Our results suggest that initial interaction of apoA-I with ABCA1 imparts a unique conformation that partially determines the in vivo metabolic fate of apoA-I, resulting in increased liver and decreased kidney catabolism as pre-beta HDL particle size increases.     

Increased cellular free cholesterol in macrophage-specific Abca1 knock-out mice enhances pro-inflammatory response of macrophages

Macrophage-specific Abca1 knock-out (Abca1(-)(M)(/-)(M)) mice were generated to determine the role of macrophage ABCA1 expression in plasma lipoprotein concentrations and the innate immune response of macrophages. Plasma lipid and lipoprotein concentrations in chow-fed Abca1(-)(M)(/-)(M) and wild-type (WT) mice were indistinguishable. Compared with WT macrophages, Abca1(-)(M)(/-)(M) macrophages had a >95% reduction in ABCA1 protein, failed to efflux lipid to apoA-I, and had a significant increase in free cholesterol (FC) and membrane lipid rafts without induction of endoplasmic reticulum stress. Lipopolysaccharide (LPS)-treated Abca1(-)(M)(/-)(M) macrophages exhibited enhanced expression of pro-inflammatory cytokines and increased activation of the NF-kappaB and MAPK pathways, which could be diminished by silencing MyD88 or by chemical inhibition of NF-kappaB or MAPK. In vivo LPS injection also resulted in a higher pro-inflammatory response in Abca1(-)(M)(/-)(M) mice compared with WT mice. Furthermore, cholesterol depletion of macrophages with methyl-beta-cyclodextrin normalized FC content between the two genotypes and their response to LPS; cholesterol repletion of macrophages resulted in increased cellular FC accumulation and enhanced cellular response to LPS. Our results suggest that macrophage ABCA1 expression may protect against atherosclerosis by facilitating the net removal of excess lipid from macrophages and dampening pro-inflammatory MyD88-dependent signaling pathways by reduction of cell membrane FC and lipid raft content.