Factors influencing the ownership and utilization of long-lasting insecticidal nets for malaria prevention in Ethiopia

Background Utilization of long-lasting insecticidal nets (LLINs) is regarded as key malaria prevention and control strategy. However, studies have reported a large gap in terms of both ownership and utilization particularly in the sub-Saharan Africa (SSA). With continual efforts to improve the use of LLIN and to progress malaria elimination, examining the factors influencing the ownership and usage of LLIN is of high importance. Therefore, the current study was conducted to examine the level of ownership and use of LLIN along with identification of associated factors at household level. Methods A cross-sectional study was conducted in Mirab Abaya District, Southern Ethiopia in June and July 2014. A total of 540 households, with an estimated 2690 members, were selected in four kebeles of the district known to have high incidence of malaria. Trained data collectors interviewed household heads to collect information on the knowledge, ownership and utilization of LLINs, which was complemented by direct observation on the conditions and use of the nets through house-to-house visit. Bivariate and multivariable logistic regression analyses were used to determine factors associated to LLIN use. Results Of 540 households intended to be included in the survey, 507 responded to the study (94.24% response rate), covering the homes of 2759 people. More than 58% of the households had family size >5 (the regional average), and 60.2% of them had at least one child below the age of 5 years. The ownership of at least one LLIN among households surveyed was 89.9%, and using at least one LLIN during the night prior to the survey among net owners was 85.1% (n = 456). Only 36.7% (186) mentioned at least as the mean of correct scores of all participants for 14 possible malaria symptoms and 32.7% (166) knew at least as the mean of correct scores of all participants for possible preventive methods. Over 30% of nets owned by the households were out of use. After controlling for confounding factors, having two or more sleeping places (adjusted odds ratio [aOR] = 2.58, 95% CI 1.17, 5.73), knowledge that LLIN prevents malaria (aOR = 2.51, 95% CI 1.17, 5.37), the presence of hanging bed nets (aOR = 19.24, 95% CI 9.24, 40.07) and walls of the house plastered or painted >12 months ago (aOR = 0.09, 95% CI 0.01, 0.71) were important predictors of LLIN utilization. Conclusions This study found a higher proportion of LLIN ownership and utilization by households than had previously been found in similar studies in Ethiopia, and in many studies in SSA. However, poor knowledge of the transmission mechanisms and the symptoms of malaria, and vector control measures to prevent malaria were evident. Moderate proportions of nets were found to be out of use or in poor repair. Efforts should be in place to maintain the current rate of utilization of LLIN in the district and improve on the identified gaps in order to support the elimination of malaria

Confirmation of a non-synonymous SNP in PNPLA8 as a candidate causal mutation for Weaver syndrome in Brown Swiss cattle

Background: Bovine progressive degenerative myeloencephalopathy (Weaver syndrome) is a neurodegenerative disorder in Brown Swiss cattle that is characterized by progressive hind leg weakness and ataxia, while sensorium and spinal reflexes remain unaffected. Although the causal mutation has not been identified yet, an indirect genetic test based on six microsatellite markers and consequent exclusion of Weaver carriers from breeding have led to the complete absence of new cases for over two decades. Evaluation of disease status by imputation of 41 diagnostic single nucleotide polymorphisms (SNPs) and a common haplotype published in 2013 identified several suspected carriers in the current breeding population, which suggests a higher frequency of the Weaver allele than anticipated. In order to prevent the reemergence of the disease, this study aimed at mapping the gene that underlies Weaver syndrome and thus at providing the basis for direct genetic testing and monitoring of today's Braunvieh/Brown Swiss herds. Results: Combined linkage/linkage disequilibrium mapping on Bos taurus chromosome (BTA) 4 based on Illumina Bovine SNP50 genotypes of 43 Weaver-affected, 31 Weaver carrier and 86 Weaver-free animals resulted in a maximum likelihood ratio test statistic value at position 49,812,384 bp. The confidence interval (0.853 Mb) determined by the 2-LOD drop-off method was contained within a 1.72-Mb segment of extended homozygosity. Exploitation of whole-genome sequence data from two official Weaver carriers and 1145 other bulls that were sequenced in Run4 of the 1000 bull genomes project showed that only a non-synonymous SNP (rs800397662) within the PNPLA8 gene at position 49,878,773 bp was concordant with the Weaver carrier status. Targeted SNP genotyping confirmed this SNP as a candidate causal mutation for Weaver syndrome. Genotyping for the candidate causal mutation in a random sample of 2334 current Braunvieh animals suggested a frequency of the Weaver allele of 0.26 %. Conclusions: Through combined use of exhaustive sequencing data and SNP genotyping results, we were able to provide evidence that supports the non-synonymous mutation at position 49,878,773 bp as the most likely causal mutation for Weaver syndrome. Further studies are needed to uncover the exact mechanisms that underlie this syndrome

Effective Rheology of Bubbles Moving in a Capillary Tube

We calculate the average volumetric flux versus pressure drop of bubbles moving in a single capillary tube with varying diameter, finding a square-root relation from mapping the flow equations onto that of a driven overdamped pendulum. The calculation is based on a derivation of the equation of motion of a bubble train from considering the capillary forces and the entropy production associated with the viscous flow. We also calculate the configurational probability of the positions of the bubbles.Comment: 4 pages, 1 figur

The Glial Scar-Monocyte Interplay: A Pivotal Resolution Phase in Spinal Cord Repair

The inflammatory response in the injured spinal cord, an immune privileged site, has been mainly associated with the poor prognosis. However, recent data demonstrated that, in fact, some leukocytes, namely monocytes, are pivotal for repair due to their alternative anti-inflammatory phenotype. Given the pro-inflammatory milieu within the traumatized spinal cord, known to skew monocytes towards a classical phenotype, a pertinent question is how parenchymal-invading monocytes acquire resolving properties essential for healing, under such unfavorable conditions. In light of the spatial association between resolving (interleukin (IL)-10 producing) monocytes and the glial scar matrix chondroitin sulfate proteoglycan (CSPG), in this study we examined the mutual relationship between these two components. By inhibiting the de novo production of CSPG following spinal cord injury, we demonstrated that this extracellular matrix, mainly known for its ability to inhibit axonal growth, serves as a critical template skewing the entering monocytes towards the resolving phenotype. In vitro cell culture studies demonstrated that this matrix alone is sufficient to induce such monocyte polarization. Reciprocal conditional ablation of the monocyte-derived macrophages concentrated at the lesion margins, using diphtheria toxin, revealed that these cells have scar matrix-resolving properties. Replenishment of monocytic cell populations to the ablated mice demonstrated that this extracellular remodeling ability of the infiltrating monocytes requires their expression of the matrix-degrading enzyme, matrix metalloproteinase 13 (MMP-13), a property that was found here to be crucial for functional recovery. Altogether, this study demonstrates that the glial scar-matrix, a known obstacle to regeneration, is a critical component skewing the encountering monocytes towards a resolving phenotype. In an apparent feedback loop, monocytes were found to regulate scar resolution. This cross-regulation between the glial scar and monocytes primes the resolution of this interim phase of spinal cord repair, thereby providing a fundamental platform for the dynamic healing response

Crystal Growth of Thiol-Stabilized Gold Nanoparticles by Heat-Induced Coalescence

A monolayer of dodecanethiol-stabilized gold nanoparticles changed into two-dimensional and three-dimensional self-organized structures by annealing at 323 K. Subsequent crystal growth of gold nanoparticles occurred. Thiol molecules, although chemisorbed, form relatively unstable bonds with the gold surface; a few thiols desorbed from the surface and oxidized to disulfides at 323 K, because the interaction energy between thiol macromolecules is larger than that between a thiol and a nanoparticle. The gold nanoparticles approached each other and grew into large single or twinned crystals because of the van der Waals attraction and the heat generated by the exothermic formation of disulfides

NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury

BACKGROUND: A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has demonstrated rapid re-expression of CSPGs at and around the lesion site. The pharmacological digestion of CSPGs in such lesion models results in substantially enhanced axonal regeneration and a significant functional recovery. The potential therapeutic relevance of interfering with CSPG expression or function following experimental injuries seems clear, however, the spatio-temporal pattern of expression of individual members of the CSPG family following human spinal cord injury is only poorly defined. In the present correlative investigation, the expression pattern of CSPG family members NG2, neurocan, versican and phosphacan was studied in the human spinal cord. METHODS: An immunohistochemical investigation in post mortem samples of control and lesioned human spinal cords was performed. All patients with traumatic SCI had been clinically diagnosed as having "complete" injuries and presented lesions of the maceration type. RESULTS: In sections from control spinal cord, NG2 immunoreactivity was restricted to stellate-shaped cells corresponding to oligodendrocyte precursor cells. The distribution patterns of phosphacan, neurocan and versican in control human spinal cord parenchyma were similar, with a fine reticular pattern being observed in white matter (but also located in gray matter for phosphacan). Neurocan staining was also associated with blood vessel walls. Furthermore, phosphacan, neurocan and versican were present in the myelin sheaths of ventral and dorsal nerve roots axons. After human SCI, NG2 and phosphacan were both detected in the evolving astroglial scar. Neurocan and versican were detected exclusively in the lesion epicentre, being associated with infiltrating Schwann cells in the myelin sheaths of invading peripheral nerve fibres from lesioned dorsal roots. CONCLUSION: NG2 and phosphacan were both present in the evolving astroglial scar and, therefore, might play an important role in the blockade of successful CNS regeneration. Neurocan and versican, however, were located at the lesion epicentre, associated with Schwann cell myelin on regenerating peripheral nerve fibres, a distribution that was unlikely to contribute to failed CNS axon regeneration. The present data points to the importance of such correlative investigations for demonstrating the clinical relevance of experimental data

6-Sulphated Chondroitins Have a Positive Influence on Axonal Regeneration

Chondroitin sulphate proteoglycans (CSPGs) upregulated in the glial scar inhibit axon regeneration via their sulphated glycosaminoglycans (GAGs). Chondroitin 6-sulphotransferase-1 (C6ST-1) is upregulated after injury leading to an increase in 6-sulphated GAG. In this study, we ask if this increase in 6-sulphated GAG is responsible for the increased inhibition within the glial scar, or whether it represents a partial reversion to the permissive embryonic state dominated by 6-sulphated glycosaminoglycans (GAGs). Using C6ST-1 knockout mice (KO), we studied post-injury changes in chondroitin sulphotransferase (CSST) expression and the effect of chondroitin 6-sulphates on both central and peripheral axon regeneration. After CNS injury, wild-type animals (WT) showed an increase in mRNA for C6ST-1, C6ST-2 and C4ST-1, but KO did not upregulate any CSSTs. After PNS injury, while WT upregulated C6ST-1, KO showed an upregulation of C6ST-2. We examined regeneration of nigrostriatal axons, which demonstrate mild spontaneous axon regeneration in the WT. KO showed many fewer regenerating axons and more axonal retraction than WT. However, in the PNS, repair of the median and ulnar nerves led to similar and normal levels of axon regeneration in both WT and KO. Functional tests on plasticity after the repair also showed no evidence of enhanced plasticity in the KO. Our results suggest that the upregulation of 6-sulphated GAG after injury makes the extracellular matrix more permissive for axon regeneration, and that the balance of different CSs in the microenvironment around the lesion site is an important factor in determining the outcome of nervous system injury

RASOnD - A comprehensive resource and search tool for RAS superfamily oncogenes from various species

<p>Abstract</p> <p>Background</p> <p>The Ras superfamily plays an important role in the control of cell signalling and division. Mutations in the Ras genes convert them into active oncogenes. The Ras oncogenes form a major thrust of global cancer research as they are involved in the development and progression of tumors. This has resulted in the exponential growth of data on Ras superfamily across different public databases and in literature. However, no dedicated public resource is currently available for data mining and analysis on this family. The present database was developed to facilitate straightforward accession, retrieval and analysis of information available on Ras oncogenes from one particular site.</p> <p>Description</p> <p>We have developed the RAS Oncogene Database (RASOnD) as a comprehensive knowledgebase that provides integrated and curated information on a single platform for oncogenes of Ras superfamily. RASOnD encompasses exhaustive genomics and proteomics data existing across diverse publicly accessible databases. This resource presently includes overall 199,046 entries from 101 different species. It provides a search tool to generate information about their nucleotide and amino acid sequences, single nucleotide polymorphisms, chromosome positions, orthologies, motifs, structures, related pathways and associated diseases. We have implemented a number of user-friendly search interfaces and sequence analysis tools. At present the user can (i) browse the data (ii) search any field through a simple or advance search interface and (iii) perform a BLAST search and subsequently CLUSTALW multiple sequence alignment by selecting sequences of Ras oncogenes. The Generic gene browser, GBrowse, JMOL for structural visualization and TREEVIEW for phylograms have been integrated for clear perception of retrieved data. External links to related databases have been included in RASOnD.</p> <p>Conclusions</p> <p>This database is a resource and search tool dedicated to Ras oncogenes. It has utility to cancer biologists and cell molecular biologists as it is a ready source for research, identification and elucidation of the role of these oncogenes. The data generated can be used for understanding the relationship between the Ras oncogenes and their association with cancer. The database updated monthly is freely accessible online at <url>http://202.141.47.181/rasond/</url> and <url>http://www.aiims.edu/RAS.html</url>.</p

Oxygen-Glucose Deprivation Induced Glial Scar-Like Change in Astrocytes

It has been demonstrated that cerebral ischemia induces astrocyte reactivity, and subsequent glial scar formation inhibits axonal regeneration during the recovery phase. Investigating the mechanism of glial scar formation will facilitate the development of strategies to improve axonal regeneration. However, an in vitro model of ischemia-induced glial scar has not yet been systematically established.In the present study, we at the first time found that oxygen-glucose deprivation (OGD) in vitro can induce rat cortical astrocytes to present characteristics of glial scar. After OGD for 6 h, astrocytes showed a remarkable proliferation following 24 h reperfusion, evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and BrdU immunocytochemistry. Meanwhile, the expression of glial fibrillary acidic protein significantly increased, so did the expression of neurocan, which is a hallmark of the glial scar. In further experiments, neurons were co-cultured with astrocytes, which had been exposed to OGD, and then the immunostaining of class III β-tubulin was carried out to assess the neurite growth. When the co-culture was performed at 48 h reperfusion of astrocytes, the neurite growth was obviously inhibited, and this inhibition could be reversed by chondroitinase ABC, which digests glycosaminoglycan chains on CSPGs, including neurocan. However, the processes of neurons were elongated, when the co-culture was performed immediately after OGD.Our results indicated that after conditioned OGD the astrocytes presented the characteristics of the glial scar, which are also comparable to the astrocytes in acute and chronic phases after cerebral ischemia in vivo. Therefore, the present system may be used as an in vitro model to explore the mechanisms underlying glial scar formation and the treatments to improve axonal regeneration after cerebral ischemia