Habitat Matters for Inorganic Carbon Acquisition in 38 Species of Red Macroalgae (Rhodophyta) from Puget Sound, Washington, USA

The ability of macroalgae to photosynthetically raise the pH and deplete the inorganic carbon pool from the surrounding medium has been in the past correlated with habitat and growth conditions. The objectives of this study were 1) to test for differences among a variety of red algal species in their ability to deplete the dissolved inorganic carbon pool (DIC) from the surrounding medium, and to utilize the HCO3- fraction of the DIC, 2) to determine whether these differences were associated with red algal habitat defined as intertidal height and subtidal depth, and/or with taxonomic affinities of the species studied (taxonomic order or family), and 3) to investigate possible within-species differences in DIC acquisition abilities in Mastocarpus papillatus, a species with a wider vertical distribution within the intertidal. No attempts were made to identify the specifics of the mechanisms used by macroalgae for dissolved inorganic carbon uptake. Measurements of pH drift were used to measure the ability of 38 red algal seaweeds to utilize bicarbonate and to deplete the DIC from seawater medium. Subtidal algae were typically restricted to the use of DIC in the form of dissolved CO2, reducing the initial DIC by only 9%. Intertidal species used both dissolved CO2 and bicarbonate, and reduced initial DIC by as much as 70%. DIC reductions and pH compensation points for the intertidal species tested were strongly correlated with their vertical zonation on the rocky shoreline. The efficiency in DIC depletion from the medium generally increased with tidal height, but species from the upper edge of the intertidal reversed the trend and demonstrated significantly lower DIC depletion abilities. This general pattern associated with tidal height was observed, not only among intertidal red algal species in general, but also among four species of the genus Porphyra (P. torta V. Krishnamurthy, P. papenfussii Krishnamurthy, P. perforata J. Agardh, P. fucicola Krishnamurthy) and among four populations of the broadly distributed species Mastocarpus papillatus (C. Agardh). The Mastocarpus observations suggest either that individuals of this species may be able to express alternate strategies for carbon acquisition, or that intertidal height may select for survivorship of genotypes with different carbon acquisition strategies. The four species of Porphyra were consistently less efficient in depleting the DIC from the medium than other macroalgal species from the same tidal height, providing the only evidence for a possible taxonomic effect on carbon acquisition. The physiological differences in DIC depletion from the medium were otherwise not related to phylogeny, tested as membership in red algal families and orders. This work suggests that the carbon acquisition strategy found in red macroalgal species may be a physiological attribute that bears important ecological and evolutionary implications

MediaDART: a decentralized framework for sharing multimedia content

This paper provides an overview of MediaDART, a framework for building online services for distributing and sharing digital media. Inspired by the participative model of Web 2.0, MediaDART relies on a scalable and decentralized architecture that can grow with the contribution of users. The architecture is based on an arbitrary number of nodes interconnected through a p2p network implementing a distributed hash table (DHT). The DHT provides resource storage and parallel resource processing for operations of feature extraction, adaptation and composition. MediaDART adopts application-level multicast based on distribution trees for delivery in streaming and implements algorithms to dynamically replicate resources across the network. The framework allows content description through user-defined tags. Tools for personalized content retrieval based on recommendation algorithms and user profiling are included too. This paper also describes two prototype applications and outlines further work.141-14

AIDS, primary health care and poverty

This paper analyzes the complex interrelation between poverty and AIDS. Poverty, in its many and diverse aspects and with its many and diverse consequences, creates a fertile breeding ground for the expansion of HIV/AIDS. In turn, HIV/AIDS, for its mode of transmission and its epidemiological features, badly affects the livelihood of its victims, their families, their entire communities and countries. Sub Saharan Africa bears the brunt of the epidemic. With about 10% of the world population, it has about 66.5 % of the world seropositive cases. In three Southern African countries the HIV prevalence in the adult population reaches or exceeds the level of 30 %. Recent WHO estimates put life expectancy in Sub Saharan Africa at about 47 years and that, without AIDS, it would be at about 62 years. The development achievements of the last decades risk being lost and the future of the continent is at risk. But numbers, alone, don't tell the whole story. They don't talk of millions of orphans, dilapidated health services, crumbling educational systems, illiteracy, gender discriminations, harmful cultural practices, uncontrolled urbanization, conflicts and civil wars, refugees and internally displaced people, entire economies on the verge of collapsing. In the rich countries, AIDS is no more a death penalty. It is a chronic disease that, although with problems, can be treated. For years the idea that the poor "had to be" excluded from the benefits of Antiretroviral Treatment (ART), simply because they are poor, has been accepted somehow passively. Things are now changing. The paper briefly touches upon ART and its implications. It is also stated that all deaths due to poverty and deprivation are unacceptable, not just those due to AIDS. The main conclusion is that the fight against HIV/AIDS is the fight against poverty. The resources to win this war are not lacking. What seems to be lacking are vision, political will and genuine interest in all human beings

Natural killer-cell immunoglobulin-like receptors trigger differences in immune response to SARS-CoV-2 infection

Background: The diversity in the clinical course of COVID-19 has been related to differences in innate and adaptative immune response mechanisms. Natural killer (NK) lymphocytes are critical protagonists of human host defense against viral infections. It would seem that reduced circulating levels of these cells have an impact on COVID-19 progression and severity. Their activity is strongly regulated by killer-cell immuno-globulin-like receptors (KIRs) expressed on the NK cell surface. The present study's focus was to investigate the impact of KIRs and their HLA Class I ligands on SARS-CoV-2 infection. Methods: KIR gene frequencies, KIR haplotypes, KIR ligands and combinations of KIRs and their HLA Class I ligands were investigated in 396 Sardinian patients with SARS-CoV-2 infection. Comparisons were made between 2 groups of patients divided according to disease severity: 240 patients were symptomatic or paucisymptomatic (Group A), 156 hospitalized patients had severe disease (Group S). The immunogenetic characteristics of patients were also compared to a population group of 400 individuals from the same geographical areas. Results: Substantial differences were obtained for KIR genes, KIR haplotypes and KIR-HLA ligand combinations when comparing patients of Group S to those of Group A. Patients in Group S had a statistically significant higher frequency of the KIR A/A haplotype compared to patients in Group A [34.6% vs 23.8%, OR = 1.7 (95% CI 1.1-2.6); P = 0.02, Pc = 0.04]. Moreover, the KIR2DS2/HLA C1 combination was poorly represented in the group of patients with severe symptoms compared to those of the asymptomatic-paucisymptomatic group [33.3% vs 50.0%, OR = 0.5 (95% CI 0.3-0.8), P = 0.001, Pc = 0.002]. Multivariate analysis confirmed that, regardless of the sex and age of the patients, the latter genetic variable correlated with a less severe disease course [ORM = 0.4 (95% CI 0.3-0.7), PM = 0.0005, PMC = 0.005]. Conclusions: The KIR2DS2/HLA C1 functional unit resulted to have a strong protective effect against the adverse outcomes of COVID-19. Combined to other well known factors such as advanced age, male sex and concomitant autoimmune diseases, this marker could prove to be highly informative of the disease course and thus enable the timely intervention needed to reduce the mortality associated with the severe forms of SARS-CoV-2 infection. However, larger studies in other populations as well as experimental functional studies will be needed to confirm our findings and further pursue the effect of KIR receptors on NK cell immune-mediated response to SARS-Cov-2 infection

Variants within the immunoregulatory CBLB gene are associated with multiple sclerosis

A genome wide association scan of ~6.6 million genotyped or imputed variants in 882 Sardinian Multiple Sclerosis (MS) cases and 872 controls suggested association of CBLB gene variants with disease, which was confirmed in 1,775 cases and 2,005 controls (overall P =1.60 × 10-10). CBLB encodes a negative regulator of adaptive immune responses and mice lacking the orthologue are prone to experimental autoimmune encephalomyelitis, the animal model of MS

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.Peer reviewe

Association of Variants in the SPTLC1 Gene With Juvenile Amyotrophic Lateral Sclerosis

Importance: Juvenile amyotrophic lateral sclerosis (ALS) is a rare form of ALS characterized by age of symptom onset less than 25 years and a variable presentation.Objective: To identify the genetic variants associated with juvenile ALS.Design, Setting, and Participants: In this multicenter family-based genetic study, trio whole-exome sequencing was performed to identify the disease-associated gene in a case series of unrelated patients diagnosed with juvenile ALS and severe growth retardation. The patients and their family members were enrolled at academic hospitals and a government research facility between March 1, 2016, and March 13, 2020, and were observed until October 1, 2020. Whole-exome sequencing was also performed in a series of patients with juvenile ALS. A total of 66 patients with juvenile ALS and 6258 adult patients with ALS participated in the study. Patients were selected for the study based on their diagnosis, and all eligible participants were enrolled in the study. None of the participants had a family history of neurological disorders, suggesting de novo variants as the underlying genetic mechanism.Main Outcomes and Measures: De novo variants present only in the index case and not in unaffected family members.Results: Trio whole-exome sequencing was performed in 3 patients diagnosed with juvenile ALS and their parents. An additional 63 patients with juvenile ALS and 6258 adult patients with ALS were subsequently screened for variants in the SPTLC1 gene. De novo variants in SPTLC1 (p.Ala20Ser in 2 patients and p.Ser331Tyr in 1 patient) were identified in 3 unrelated patients diagnosed with juvenile ALS and failure to thrive. A fourth variant (p.Leu39del) was identified in a patient with juvenile ALS where parental DNA was unavailable. Variants in this gene have been previously shown to be associated with autosomal-dominant hereditary sensory autonomic neuropathy, type 1A, by disrupting an essential enzyme complex in the sphingolipid synthesis pathway.Conclusions and Relevance: These data broaden the phenotype associated with SPTLC1 and suggest that patients presenting with juvenile ALS should be screened for variants in this gene.</p

Official Development Assistance: a Critical Overview

Whereas 22 developed countries have pledged to contribute a paltry 0.7% of their GDP in form of Official Development Assistance (ODA) to developing countries, after 40 years of the commitment, only five countries have come close to that target. This paper argues that even then, the assistance is provided inefficiently since most of it is spent as unsolicited expensive Technical Assistance or repatriated in form of input purchase conditionalities. The paper also argues that ODA figures are artificially inflated by donors including forgiven debts as new assistance. It traces the recent history of development assistance from the Marshall Plan to the Paris Declaration on Aid Effectiveness. It singles out aid conditionalities as "master-student arrogance". It also criticises endless postponement of deadlines for achieving human development goals as tantamount to goal-shifting. Finally, it concludes that external aid cannot deliver a country from poverty, since the amounts committed are too small, the commitment too little, the donor agendas too many, and argues that only fair trade can contribute meaningfully to lifting the poor in recipient countries to acceptable levels of human development