Cryonics for all?

In fascinating recent work, some philosophers have argued that it would be morally permissible and prudentially rational to sign up for cryonics—if you can afford the price tag of the procedure. In this paper I ask: why not share the elixir of extended life with everyone? Should governments financially support, positively encourage, or even require people to undergo cryonics? From a general principle of beneficence, I construct a formal argument for cryonics promotion policies. I consider the objection that a subset of these policies would violate autonomy, but I argue that—to the contrary—considerations of autonomy weigh in their favour. I then consider objections based on cost and population, but argue that neither is fatal. Finally, I raise the objection that I believe poses the most serious challenge: that those who revive the cryonically preserved might inflict suffering upon them.     

Chemokines: extracellular messengers for all occasions?

Movement of leukocytes from peripheral blood into tissues, also called leukocyte extravasation, is absolutely essential for immunity in higher organisms. Over the past decade, our understanding of the molecular mechanisms involved in white blood cell extravasation during both normal immune surveillance and the generation of protective immune responses has taken a great leap forward with the discovery of the chemokine gene superfamily. Chemokines are low-molecular-weight cytokines whose major collective biological activity appears to be that of chemotaxis of both specific and overlapping subsets of leukocytes. They are therefore likely to play a critical role in the directed movement of leukocytes from the bloodstream into tissue. These molecules are almost exclusively secreted and act as extracellular messengers for the immune system. However, emerging data also show that various members of the chemokine gene superfamily exert other biological effects outside the immune system. All nucleated cells and all tissues examined to date are capable of expressing at least some chemokines, and it seems likely therefore that by the time all the chemokines are identified, and all their biological functions elucidated, we will find that, as a family, these molecules perform an extracellular messenger role in all tissues and systems of the body.     

Need for and Access to Health Care and Medicines: Are There Gender Inequities?

Objective

Differences between women and men in political and economic empowerment, education, and health risks are well-documented. Similar gender inequities in access to care and medicines have been hypothesized but evidence is lacking.

Methods

We analyzed 2002 World Health Survey data for 257,922 adult respondents and 80,932 children less than 5 years old from 53 mostly low and middle-income countries. We constructed indicators of need for, access to, and perceptions of care, and we described the number of countries with equal and statistically different proportions of women and men for each indicator. Using multivariate logistic regression models, we estimated effects of gender on our study outcomes, overall and by household poverty.

Findings

Women reported significantly more need for care for three of six chronic conditions surveyed, and they were more likely to have at least one of the conditions (OR 1.41 [95% CI 1.38, 1.44]). Among those with reported need for care, there were no consistent differences in access to care between women and men overall (e.g., treatment for all reported chronic conditions, OR 1.00 [0.96, 1.04]) or by household poverty. Of concern, access to care for chronic conditions was distressingly low among both men and women in many countries, as was access to preventive services among boys and girls less than 5 years old.

Conclusions

These cross-country results do not suggest a systematic disadvantage of women in access to curative care and medicines for treating selected chronic conditions or acute symptoms, or to preventive services among boys and girls.     

Fungal septins: one ring to rule it all?

Septins are a conserved family of GTP-binding proteins found in living organisms ranging from yeasts to mammals. They are able to polymerize and form hetero-oligomers that assemble into higher-order structures whose detailed molecular architecture has recently been described in different organisms. In Saccharomyces cerevisiae, septins exert numerous functions throughout the cell cycle, serving as scaffolds for many different proteins or as diffusion barriers at the bud neck. In other fungi, septins are required for the proper completion of diverse functions such as polarized growth or pathogenesis. Recent results from several fungi have revealed important differences in septin organization and regulation as compared with S. cerevisiae, especially during Candida albicans hyphal growth and in Ashbya gossypii. Here we focus on these recent findings, their relevance in the biology of these eukaryotes and in consequence the “renaissance” of the study of septin structures in cells showing a different kind of morphological behaviour.     

One ring to rule them all? Another cellular responsibility for PCNA

To prevent duplication or loss of genomic regions during DNA replication, it is essential that the entire genome is copied precisely once every S phase. Cells achieve this by mutually exclusive regulation of origin firing and licensing. A crucial protein that is involved in origin licensing is chromatin licensing and DNA replication factor 1 (CDT1) and, therefore, activity of this protein must be strictly controlled. Four recent articles have demonstrated that proliferating cell nuclear antigen (PCNA), an essential sliding clamp used in replication and DNA repair, has a crucial role in this process by mediating the proteasomal degradation of CDT1.     

Parkinson's disease: one biochemical pathway to fit all genes?

Although originally discounted, hereditary factors have emerged as the focus of research in Parkinson's disease (PD). Genetic studies have identified mutations in alpha-synuclein and ubiquitin C-terminal hydrolase as rare causes of autosomal dominant PD and mutations in parkin as a cause of autosomal recessive PD. Functional characterization of the identified disease genes implicates the ubiquitin-mediated protein degradation pathway in these hereditary forms of PD and also in the more common sporadic forms of PD. Subsequent identification of further loci in familial PD and diverse genetic factors modulating the risk for sporadic PD point to substantial genetic heterogeneity in the disease. Thus, new candidate genes are expected to encode proteins either involved in ubiquitin-mediated protein degradation or sequestrated in intracytoplasmic protein aggregations. Future identification of disease genes is required to confirm this hypothesis, thereby unifying the clinical and genetic heterogeneity of PD, including the common sporadic form of the disease, by one biochemical pathway.     

Pulmonary vein isolation: do all roads lead to Rome?

Pulmonary vein isolation (PVI) for the treatment of atrial fibrillation (AF) appears to be here to stay. In just a few years since the landmark publications by Haissaguerre and Pappone, countless variations on the theme of ostial or antral PVI, with or without additional lines or point lesions, have been published. The procedure has found its way into daily practice and international guidelines, and is currently the most performed ablation in the Netherlands.     

Access and benefit-sharing: what indicators to measure ‘success’?

We examine challenges with measuring ‘success’ in access and benefit-sharing (ABS) of biological resources. We note a lack of indicators and draw on Pacific patent landscaping, ABS case studies, and research permit figures to highlight that ABS systems are functioning somewhat, although they are often not meeting expectations.     

Will tuberculosis become resistant to all antibiotics?

The discovery of high prevalences of antibiotic resistance in some pathogens, in some parts of the world, has provoked fears of a widespread loss of drug efficacy. Here, we use a mathematical model to investigate the evolution of resistance to four major anti-tuberculosis drugs (isoniazid, rifampicin, ethambutol and streptomycin) in 47 sites around the world. The model provides a new method of estimating the relative risk of treatment failure for patients carrying drug-resistant strains and the proportion of patients who develop resistance after failing treatment. Using estimates of these two quantities together with other published data, we reconstructed the epidemic spread of isoniazid resistance over the past 50 years. The predicted median prevalence of resistance among new cases today was 7.0% (range 0.9-64.3%), close to the 6.3% (range 0-28.1%) observed. Predicted and observed prevalences of resistance to isoniazid plus rifampicin (multidrug-resistant or MDR-TB) after 30 years of combined drug use were also similar, 0.9% (0.1-5.9%) and 1.0% (range 0-14.1%), respectively. With current data, and under prevailing treatment practices, it appears that MDR-TB will remain a localized problem, rather than becoming a global obstacle to tuberculosis control. To substantiate this result, further measurements are needed of the relative fitness of drug-resistant strains.