Dairy manure pellets and palm oil mill effluent as alternative nutrient sources in cultivating Sporosarcina pasteurii for calcium carbonate bioprecipitation

Microbially induced carbonate precipitation (MICP) is a process that hydrolysis urea by microbial urease to fill the pore spaces of soil with induced calcium carbonate (CaCO₃) precipitates, which eventually results in improved or solidified soil. This research explored the possibility of using dairy manure pellets (DMP) and palm oil mill effluent (POME) as alternative nutrient sources for Sporosarcina pasteurii cultivation and CaCO₃ bioprecipitation. Different concentrations (20–80 g l⁻¹) of DMP and POME were used to propagate the cells of S. pasteurii under laboratory conditions. The measured CaCO₃ contents for MICP soil specimens that were treated with bacterial cultures grown in DMP medium (60%, w/v) was 15·30 ± 0·04 g ml⁻¹ and POME medium (40%, v/v) was 15·49 ± 0·05 g ml⁻¹ after 21 days curing. The scanning electron microscopy showed that soil treated with DMP had rhombohedral structure-like crystals with smooth surfaces, whilst that of POME entailed ring-like cubical formation with rough surfaces Electron dispersive X-ray analysis was able to identify a high mass percentage of chemical element compositions (Ca, C and O), whilst spectrum from Fourier-transform infrared spectroscopy confirmed the vibration peak intensities for CaCO₃. Atomic force microscopy further showed clear topographical differences on the crystal surface structures that were formed around the MICP treated soil samples. These nutrient sources (DMP and POME) showed encouraging potential cultivation mediums to address high costs related to bacterial cultivation and biocementation treatment.     

Über die Rolle des Callciums im leben der Zelle auf Grund von Versuchen an Micrasterias

Ohne ZusammenfassungMit 18 Textabbildungen.     

Serious adverse events following treatment of visceral leishmaniasis: A systematic review and meta-analysis

BackgroundDespite a historical association with poor tolerability, a comprehensive review on safety of antileishmanial chemotherapies is lacking. We carried out an update of a previous systematic review of all published clinical trials in visceral leishmaniasis (VL) from 1980 to 2019 to document any reported serious adverse events (SAEs).MethodsFor this updated systematic review, we searched the following databases from 1^st Jan 2016 through 2^nd of May 2019: PUBMED, Embase, Scopus, Web of Science, Cochrane, clinicaltrials.gov, WHO ICTRP, and the Global Index Medicus. We included randomised and non-randomised interventional studies aimed at assessing therapeutic efficacy and extracted the number of SAEs reported within the first 30 days of treatment initiation. The incidence rate of death (IRD) from individual treatment arms were combined in a meta-analysis using random effects Poisson regression.ResultsWe identified 157 published studies enrolling 35,376 patients in 347 treatment arms. Pentavalent antimony was administered in 74 (21.3%), multiple-dose liposomal amphotericin B (L-AmB) in 52 (15.0%), amphotericin b deoxycholate in 51 (14.7%), miltefosine in 33 (9.5%), amphotericin b fat/lipid/colloid/cholesterol in 31 (8.9%), and single-dose L-AmB in 17 (4.9%) arms. There was a total of 804 SAEs reported of which 793 (including 428 deaths) were extracted at study arm level (11 SAEs were reported at study level only). During the first 30 days, there were 285 (66.6%) deaths with the overall IRD estimated at 0.068 [95% confidence interval (CI): 0.041–0.114; I² = 81.4%; 95% prediction interval (PI): 0.001–2.779] per 1,000 person-days at risk; the rate was 0.628 [95% CI: 0.368–1.021; I² = 82.5%] in Eastern Africa, and 0.041 [95% CI: 0.021–0.081; I² = 68.1%] in the Indian Subcontinent. In 21 study arms which clearly indicated allowing the inclusion of patients with HIV co-infections the IRD was 0.575 [95% CI: 0.244–1.355; I² = 91.9%] compared to 0.043 [95% CI: 0.020–0.090; I² = 62.5%] in 160 arms which excluded HIV co-infections.ConclusionMortality within the first 30 days of VL treatment initiation was a rarely reported event in clinical trials with an overall estimated rate of 0.068 deaths per 1,000 person-days at risk, though it varied across regions and patient populations. These estimates may serve as a benchmark for future trials against which mortality data from prospective and pharmacovigilance studies can be compared. The methodological limitations exposed by our review support the need to assemble individual patient data (IPD) to conduct robust IPD meta-analyses and generate stronger evidence from existing trials to support treatment guidelines and guide future research.     

Genetic inactivation of RIP1 kinase activity in rats protects against ischemic brain injury

RIP1 kinase-mediated inflammatory and cell death pathways have been implicated in the pathology of acute and chronic disorders of the nervous system. Here, we describe a novel animal model of RIP1 kinase deficiency, generated by knock-in of the kinase-inactivating RIP1(D138N) mutation in rats. Homozygous RIP1 kinase-dead (KD) rats had normal development, reproduction and did not show any gross phenotypes at baseline. However, cells derived from RIP1 KD rats displayed resistance to necroptotic cell death. In addition, RIP1 KD rats were resistant to TNF-induced systemic shock. We studied the utility of RIP1 KD rats for neurological disorders by testing the efficacy of the genetic inactivation in the transient middle cerebral artery occlusion/reperfusion model of brain injury. RIP1 KD rats were protected in this model in a battery of behavioral, imaging, and histopathological endpoints. In addition, RIP1 KD rats had reduced inflammation and accumulation of neuronal injury biomarkers. Unbiased proteomics in the plasma identified additional changes that were ameliorated by RIP1 genetic inactivation. Together these data highlight the utility of the RIP1 KD rats for target validation and biomarker studies for neurological disorders.Subject terms: Cell death in the nervous system, Diseases of the nervous system     

Trem2 restrains the enhancement of tau accumulation and neurodegeneration by β-amyloid pathology

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Relationship between the GTPase,metal-binding,and dimerization activities of <Emphasis Type="Italic">E. coli</Emphasis> HypB

Biosynthesis of the metallocenter in the active site of the [NiFe] hydrogenase enzyme requires the accessory protein HypB, which is a metal-binding GTPase. In this study, the interplay between the individual activities of Escherichia coli HypB was examined. The full-length protein undergoes nucleotide-responsive dimerization that is disrupted upon mutation of L242 and L246 to alanine. This mutant HypB is monomeric under all of the conditions investigated but the inability of L242A/L246A HypB to dimerize does not abolish its GTPase activity and the monomeric protein has metal-binding behavior similar to that of wild-type HypB. Furthermore, expression of L242A/L246A HypB in vivo results in hydrogenase activity that is approximately half of the activity produced by the wild-type control, suggesting that dimerization of HypB does not have a critical role in the hydrogenase maturation pathway. In contrast, the GTPase activity of HypB is modulated by metal loading of the protein. These results provide insight into the role of HypB in hydrogenase biosynthesis.     

Living Monoplacophora: morphological conservatism or recent diversification?

Kano, Y., Kimura, S., Kimura, T. & Warén, A. (2012) Living Monoplacophora: morphological conservatism or recent diversification? —Zoologica Scripta, 41, 471–488. The molluscs of the class Monoplacophora are classic and probably the most striking case of a ‘living fossil’ in the deep sea. Until the discovery of the first living specimens in 1950s, the group was thought to be extinct since the Devonian period, almost 400 million years ago. Morphological conservatism over a long span of time in a ‘living‐fossil’ lineage may theoretically result in distant but closely resembling taxa, and this idea apparently led some authors to recognise as many as six families and three superfamilies for less than three dozen living monoplacophoran species. However, no genetic or fossil data have been available regarding the history of their diversification. Here we describe Veleropilina seisuimaruae sp. n., the first member of the class from the north‐western Pacific, based on the shell, radular and anatomical characteristics. Phylogenetic analyses of 6‐kb DNA sequences estimate that the divergence of V. seisuimaruae and Laevipilina hyalina, the only other monoplacophoran available for genetic studies, dates back only to the Late Cretaceous, despite their significant morphological differences among the living members of the class. The recent Monoplacophora might have radiated fairly recently from a cryptic lineage with ordinary rates of morphological evolution, possibly after the global deep‐sea anoxia at the Cenomanian/Turonian boundary.     

Eulimid gastropods parasitic on echinoderms in the New Zealand region

Abstract

Eulimindae (Prosobranchia) of the New Zealand region that parasitise echinoderms are recorded and discussed. Fuscapex ophioacanthicola n.gen. & sp. is parasitic on Ophioacantha sp., Ophieulima fuscoapicata n.sp. is a parasite of Ophioactis profundi Lütken & Mortensen, Punctifera ophiomoefrae n.gen. & sp. lives partly buried among the radial shields of Ophiomoeris projecta Matsumato, and Stilapex sp. is recorded, but not described, from Ophiothrix oliveri Benham (all hosts ophiuroids). Stilifer sp. lives in galls in an undescribed oreasterid (Asteroidea). Annulobalcis marshalli n.sp. is described from Crotalometra rustica (A. H. Clark) (Crinoidea). Eulima infrapatula Murdoch & Suter is transferred to Sabinella Monterosato and recorded from Ogmocidaris benhami Mortensen; Fusceulima goodingi n.sp. is described from Centrostephanus rodgersi (A. Agassiz) (both hosts echinoids). Two earlier records of sea urchin parasites from New Zealand are discussed, and the species are referred to Pelseneeria.     

Multiple sclerosis risk gene Mertk is required for microglial activation and subsequent remyelination

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