A Chromosome Study of Chlorophytum Elatum

The spider plant, Chlorophytum elatum R. Br., a member of the family Liliaceae, is a native of South Africa. It has been propagated almost exclusively by vegetative means and it is now grown widely over the world as an ornamental plant. Many studies by other workers have revealed that with only two exceptions all species in the genus Chlorophytum have somatic chromosome numbers that are multiples of seven, ranging from 14 to 56 (c.f. Darlington and Wiley, 1955). Although the chromosome number of Chlorophytum elatum has ·been reported to be 2N = 28 (Sato, 1942; Baldwin and Speese, 1951) information regarding its karyotype is not complete and meiotic behavior is still lacking. Storey (1968), after studying the mitotic phenomenon in roottip cells, suggested that this species might be an autotetraploid with a basic number X = 7. However, he failed to study the meiotic chromosomes which would be essential in order to verify his assumption. The clone of Chlorophytum elatum, which has been maintained in the Botany Greenhouse, was noted to show some degree of sterility. Preliminary observations of the pollen indicated that about 25 percent of the grains were non-stainable and irregular in shape. This implied that either a change in chromosome number or an alteration of chromosome structure might occur in this particular clone such as was observed in other genera by Carnahan and Hill (1962); Dhaliwal, Pollard, and Lorz (1962); Doughty (1936); Honma (1968); Kreft (1968); Sutton (1937); Thomas (1960); Upcott and Lacour (1936); Upcott (1937); and Whitaker (1935). This study was undertaken to ascertain the karyotype of Chlorophytum elatum and to study the meiotic chromosome behavior. A karyotypic analysis supported by a study of the behavior of chromosomes during diakinesis and/or metaphase I was made to determine the ploidy of this clone. The study of the meiotic chromosome behavior at later stages of meiosis along with a karyotypic analysis was made to find an explanation for the clone\u27s sterility

Sampling Theorem and Discrete Fourier Transform on the Riemann Sphere

Using coherent-state techniques, we prove a sampling theorem for Majorana's (holomorphic) functions on the Riemann sphere and we provide an exact reconstruction formula as a convolution product of $N$ samples and a given reconstruction kernel (a sinc-type function). We also discuss the effect of over- and under-sampling. Sample points are roots of unity, a fact which allows explicit inversion formulas for resolution and overlapping kernel operators through the theory of Circulant Matrices and Rectangular Fourier Matrices. The case of band-limited functions on the Riemann sphere, with spins up to $J$, is also considered. The connection with the standard Euler angle picture, in terms of spherical harmonics, is established through a discrete Bargmann transform.Comment: 26 latex pages. Final version published in J. Fourier Anal. App

Structural similarity-based predictions of protein interactions between HIV-1 and Homo sapiens

Abstract Background In the course of infection, viruses such as HIV-1 must enter a cell, travel to sites where they can hijack host machinery to transcribe their genes and translate their proteins, assemble, and then leave the cell again, all while evading the host immune system. Thus, successful infection depends on the pathogen's ability to manipulate the biological pathways and processes of the organism it infects. Interactions between HIV-encoded and human proteins provide one means by which HIV-1 can connect into cellular pathways to carry out these survival processes. Results We developed and applied a computational approach to predict interactions between HIV and human proteins based on structural similarity of 9 HIV-1 proteins to human proteins having known interactions. Using functional data from RNAi studies as a filter, we generated over 2000 interaction predictions between HIV proteins and 406 unique human proteins. Additional filtering based on Gene Ontology cellular component annotation reduced the number of predictions to 502 interactions involving 137 human proteins. We find numerous known interactions as well as novel interactions showing significant functional relevance based on supporting Gene Ontology and literature evidence. Conclusions Understanding the interplay between HIV-1 and its human host will help in understanding the viral lifecycle and the ways in which this virus is able to manipulate its host. The results shown here provide a potential set of interactions that are amenable to further experimental manipulation as well as potential targets for therapeutic intervention

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Global injury morbidity and mortality from 1990 to 2017 : results from the Global Burden of Disease Study 2017

Correction:Background Past research in population health trends has shown that injuries form a substantial burden of population health loss. Regular updates to injury burden assessments are critical. We report Global Burden of Disease (GBD) 2017 Study estimates on morbidity and mortality for all injuries. Methods We reviewed results for injuries from the GBD 2017 study. GBD 2017 measured injury-specific mortality and years of life lost (YLLs) using the Cause of Death Ensemble model. To measure non-fatal injuries, GBD 2017 modelled injury-specific incidence and converted this to prevalence and years lived with disability (YLDs). YLLs and YLDs were summed to calculate disability-adjusted life years (DALYs). Findings In 1990, there were 4 260 493 (4 085 700 to 4 396 138) injury deaths, which increased to 4 484 722 (4 332 010 to 4 585 554) deaths in 2017, while age-standardised mortality decreased from 1079 (1073 to 1086) to 738 (730 to 745) per 100 000. In 1990, there were 354 064 302 (95% uncertainty interval: 338 174 876 to 371 610 802) new cases of injury globally, which increased to 520 710 288 (493 430 247 to 547 988 635) new cases in 2017. During this time, age-standardised incidence decreased non-significantly from 6824 (6534 to 7147) to 6763 (6412 to 7118) per 100 000. Between 1990 and 2017, age-standardised DALYs decreased from 4947 (4655 to 5233) per 100 000 to 3267 (3058 to 3505). Interpretation Injuries are an important cause of health loss globally, though mortality has declined between 1990 and 2017. Future research in injury burden should focus on prevention in high-burden populations, improving data collection and ensuring access to medical care.Peer reviewe