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Dissapointed with Papers2

Why, on Earth, would you release an upgrade from a popular software, only for a limited number of users because your new, improved, released software supports only the last operative system? Why the people behind Papers released the long-long-long time awaited Papers2 only for Snow Leopard Users?
I was recently reading a post regarding why Mac users still use Leopard instead of Snow Leopard. Lack of time to make the upgrade, the sense of the upgrade being unnecessary, specially considering that you have to pay for the upgrade, and reports about several bugs and incompatibilities, lead users so use Leopard even today. Most of my scientists friends are Leopard users, and also Papers1.x users, and I believe that they are happy. Despite the lack of features awaited for a long time. Even considering that Mendeley is free and always improving. And considering that, for example, Mendeley Lite for iPad is free, in contrast to Papers for iPad (which, by the way, still lacks many features).
But I have been a strong supporter of Papers. I truly believed that, somehow, old Papers1.x users were going to be awarded because of their loyalty. But the upgrade price seems to be a barrier for many, specially for students (and I believe that the new Mac-Student users will turn undoubtedly to Mendeley and Endnote), and to me (and I am pretty sure that for many others too), the need of having Snow Leopard puts another big issue to deal with.
Also, some reports about missing features, bugs and others (see The only explanation I found regarding this “hard” decision is:

Unfortunately Papers2 requires 10.6. This was a hard decision, because we know we still have a small percentage of Papers1 users running OS X Leopard 10.5. However, supporting 10.5 had also a lot of technical consequences. In particular, with OS X Lion 10.7 coming soon, we might have had to cut 10.5 support later, which would have been much more difficult to do on paying costumers.

Note of course that your copy of Papers1 will still work the exact same way as it does today on 10.5 for as long as needed.

I believe that the company does not care about loyal, old users of Papers. They say the percentage of Leopard users is small. In my experience, this percentage is pretty close to 100% (maybe because I am in a small, less-developed country, I don’t know), but this only decision is enough to me to decide not to upgrade to Papers2, and I recommend to you to do the same.

In the future, I will be featuring new softwares and tools for scientists, to compensate somehow this huge turn-off.

The most successful post: Paper versus Mendeley, Zotero and stuff.

I am really surprised. When I started this blog, I wanted to share my thoughts about science, about being scientific, about research… and also about Mac in research. When I began to use Mac, it was difficult to me because I didn’t knew so much about software, tools, and so. And then, once, I wrote a post, almost like a review, about software to manage papers and references.

To date, it is the most visited post. I can imagine that many people are looking for information about which software is best for their needs. I never intended to make an explicit publicity on a specific software. I just wanted to express my experience about using those softwares.

Now, I want to make some updates to that post, and about managing references in Mac.

1. About Mendeley: I consider myself a reasonable person, specially being a scientist. Therefore, when a new version of Mendeley is released, I install it and try to use it. But, a few minutes later, I send the program to the Trash. Even more, when a fellow ask me about a software to manage papers and references, I ask: “Mac or Windows?” If the response is “Windows”, then I answer: “Give a look to Mendeley. Give it a try”. Almost every time, my friend returns, days later, and say to me “I uninstalled Mendeley. It ‘s just… complicated”.

It seems that, for many people, Mendeley is slow, complicated, and inefficient. Besides, it’s a huge program, considering the lack of remarkable features inside it. I really want Mendeley being a good software, but the opinion of my friends is the same as mine.

b) About Papers: I love Papers. It’s my software to manage my articles. But I feel that, since a long time, the team behind Papers just relaxes. There is no real improvement in every new version of Papers; only the typical “a bug is fixed when you make that-thing-that-you-do once every two years”, and no real improvement in metadata retrieval. I paid for Papers, and if a new version with real improvements in metadata retrieval from the journals, a good system for managing a bibliography with integration woth Word and Pages, and with new tools for making annotations in the articles, I will be glad to pay for a new release. But, in summary, I feel that Papers just got delayed in time.

c) About Zotero: One day, I received that message: “A new version of Zotero….” Of course, as an obedient fan of Zotero, I installed the new version… And I never could use Zotero again. I needed a new version of the Word toolbar. It didn’t work. I tried to go back to the old version of Zotero. Nothing. Also, the Word for Mac is awful. Then I got a huge amount of work, and I never looked back to Zotero. I need more time to solve the problem, but my feelings about Zotero are not optimistic.

That’s all I have to say about this topic at this moment. If you want to know more about bibliographic management, you should read this post.

The Red Queen hypothesis in a glass
What factors predominate in evolution? In daily life, the constant evolution of our lives is influenced by our conditions and by external factors. If I want to build a house with my own hands, I have to consider my abilities, some of which are genetic (I am small, thin and I am not strong, so I can’t carry heavy materials), and also I have to check how many money I can spend; hence, the “evolution” of the house, sort of, depends on both factors.

Two hypothesis, the “Red Queen” and the “Court Jester”, view evolution in these terms [1]. The Red Queen hypothesis view evolution as a balance of biotic (intrinsic) pressures, whereas the Court Jester model propose that evolution, speciation and extinction rarely happen except in response to unpredictable changes in the physical environment. Finally, it seems reasonable that evolution proceeds as a mixture of both models, where the Court Jester model operates in a time scale far longer than the Red Queen. Locally, in an ecological niche, the competition (biotic factor) between events en species shapes the local evolution, but in a larger scale, such as earthquakes, rise of mountains, and separation of physical spaces, provide a definitive barrier shaping long-term evolution, although events such as migration in birds and migration between continents should be taken into account.

The Court Jester model seems more logical to be imagined. Darwin viewed evolution in terms of biotic factors, but in his journeys, he observed marked differences in similar species in long distances, being islands a hallmark of evolutionary observation. But the Red Queen hypothesis, in biological terms, remained a challenge to be resolved in a laboratory. In a recent paper published in Nature [2], Paterson and coworkers provided a genetic evidence for the Red Queen hypothesis, using a smart experimental design. They used co-cultures of the bacterium Pseudomonas fluorescens and its viral phage Φ2. The molecular evolution rate in the phage was higher when both bacterium and phage coevolved with each other that when phage evolved against a constant host genotype. Remarkably, the genes that most rapidly evolved were involved in host infection, after 12 serial transfers (being each transfer every 48 hours). Consequently, coevolved phage populations varied in the range and identity of host genotypes that they were able to infect, but phage from evolved populations failed to infect any coevolved hosts.

How fast a bacterium can coevolve inside a human organism? For example, in a hospital, there is a spreading of infectious bacteria. Could be possible a coevolution of the microorganism with its host, allowing the mutation and adaptation of the bacteria in order to be able to infect more hosts? It will be interesting the extrapolation of the findings from Paterson and coworkers, at the clinical level. An example is provided by a brief review in PLoS Genetics [3]. Neisseria meningitidis, a major cause of morbidity and mortality in childhood, in a lapse of three decades of observation showed little variation, but a few loci showed variation, including the gene coding for a transferrin binding protein (tbpB). However, it seems that the genetic variation occurs at expenses of the “transmission fitness”.  It will be interesting to see if this technique can be improved to study more complex and bigger “cosmos” and specially for disease-causing bacterium, or viruses.


[1] Benton MJ (2009). The Red Queen and the Court Jester: species diversity and the role of biotic and abiotic factors through time. Science (New York, N.Y.), 323 (5915), 728-32 PMID: 19197051

[2] Paterson S, Vogwill T, Buckling A, Benmayor R, Spiers AJ, Thomson NR, Quail M, Smith F, Walker D, Libberton B, Fenton A, Hall N, & Brockhurst MA (2010). Antagonistic coevolution accelerates molecular evolution. Nature, 464 (7286), 275-8 PMID: 20182425

[3] Falush D (2009). Toward the use of genomics to study microevolutionary change in bacteria. PLoS genetics, 5 (10) PMID: 19855823

Milk, Prions and Evolution

ResearchBlogging.orgPrion protein (PrP) is the focus of some neurodegenerative diseases. It is believed that misfolded prion protein (PrPsc, or “scrapie”) is the infectious agent responsible for bovine spongiform encephalopathy (BSE), and Creutzfeldt-Jacob disease (CJD), among others. PrPsc propagates by conversion of normal (healthy) prion protein (PrPc).

Several questions arise in the research community. Two of them are: a) can prions be transmitted from domestic animals into humans, and b) how the prion protein propagates inside a healthy subject. Food safety is a major concern. Milk and their derivatives are a subject of study, because of their wide consumption in most countries. A study [1] from Didier and coworkers shows that the normal prion protein is detected in mammary gland and milk fractions of cow, goat and sheep. PrPc protein is detected in all milk fractions (skimmed milk, acid whey, cream) in goat and sheep. Although the authors failed to detect PrPc in bovine milk, they refer to other study that successful detected the protein in bovine milk using a different approach. Some conclusions of this study are that analytical methods to detect the prion protein should be improved (hopefully, at an industrial scale), to avoid the variability between studies, specially considering the high levels of prion protein detected in cream fractions and the widespread use of cream in cooking.

Scrapie in milk?

Another conclusion is that the prion protein exist at low levels in mammary gland and milk. Even detecting PrPc in milk requires hard work (enrichment of protein concentration, for example). But someone expect that PrPsc should exist at even lower levels, specially in asymptomatic animals. Then, PrPsc can be undetected in an industrial quality control. What happens if the common assumption that infectious prion protein is not present in milk is wrong? There is evidence of infectious prion transmission via milk; Timm Konold and colleagues published evidence in lambs fed with infected and healthy milk, but using lambs from a genotype with high susceptibility to scrapie [2], observing high levels of infection. Thinking in human population, if  populations with genetic susceptibility to scrapie are identified, then health measures should be implemented in those populations to avoid the exposure to potentially contaminated milk and cream.

Once inside the cell, then what?

A few days ago, a comment in Science raised the question  “What makes a prion infectious?” [3]. The article referred to two papers published recently. One of them raises interesting questions regarding the possibility of disease development after drinking contaminated milk, for example. A research team from the Department of Infectology in the Scripps Institute, showed that prions in cell culture are able to “evolve” [4]. Prions, viewed as infectious agents, exists as strains, which are a specific conformer of the protein, and they are able to multimerize forming seeds. One hypothesis, called “protein-only”, assumes that each strain is associated with a different conformer of PrPsc, and the infectious agent is composed of a misfolded conformer exclusively (without cofactors). Many strains can exist, since many conformers are able to arise from PrPc misfolding. Experiments from the work of Li and colleagues shows that, indeed, these strains exist, and they were able to identify prions strains sensitive to swainsonine (inhibitor of the formation of N-linked glycans). In a series of experiments they showed that the strains identified in a time-lapse isolated from a cell line infected with a brain homogenate changed over time: in the first days, they identified swa-resistant strains (and competent for R33, a neuroblastoma-derived cell line), but then they identified swa-insensitive and R33-incompetent, after they transferring to PK1 cells. These and remaining experiments suggests that the prion population changed over time, and there are different strains that can “compete” if the growth conditions are advantageous to a specific strain.The authors, based in their results, conclude that prions show the hallmarks of Darwinian evolution: they are subject to mutation and to selective amplification. Obviously, these findings are relevant to Medicine, since drug discovery should consider the fact that, in disease conditions, the raise of a infectious prion can lead to mutation (more likely by binding of a prion to some cellular cofactor leading to a small variations in the misfolded structure) of some monomers, causing strain evolution, some of which can growth in the presence of some drug, replace the remaining strains and lead to resistance.

It is evident that we are far from understand the biochemical and molecular foundations of scrapie disease and mechanism, and the new evidence suggest a complex scenario, specially regarding to the deveolpment of new drugs to fight the clinical symptoms and the CJD and BSE diseases.


[1] Didier A, Gebert R, Dietrich R, Schweiger M, Gareis M, Märtlbauer E, & Amselgruber WM (2008). Cellular prion protein in mammary gland and milk fractions of domestic ruminants. Biochemical and biophysical research communications, 369 (3), 841-4 PMID: 18325321

[2] Konold T, Moore SJ, Bellworthy SJ, & Simmons HA (2008). Evidence of scrapie transmission via milk. BMC veterinary research, 4 PMID: 18397513

[3] Supattapone S (2010). Biochemistry. What makes a prion infectious? Science (New York, N.Y.), 327 (5969), 1091-2 PMID: 20185716

[4] Li J, Browning S, Mahal SP, Oelschlegel AM, & Weissmann C (2010). Darwinian evolution of prions in cell culture. Science (New York, N.Y.), 327 (5967), 869-72 PMID: 20044542

Earthquake in Chile and Science

Four days later, I finally have internet connection in my house. I am surfing the web, watching photos from my country. As you probably know, an earthquake stroke Chile at 3:34 am, February 27. It was 8.8 in the Ritcher scale, according to the U.S. Geological Survey Program. The second most strong earthquake in Chilean history (whereas the first most strong earthquake was in Valdivia, also in Chile, 1960, the highest earthquake in history).

The devastation in Chile is overwhelming. More than 720 deaths (and rising), 500 injured people, more than half of the country striked by the earthquake, and thousands of houses and buildings falling apart. The effects of the earthquake is big; tsunamis crashed over chilean cities, destroying them. The tsunamis reached Australia, Japan and Hawaii.

As a science’s blog, I have to say something about the effects of this earthquake over research. Preliminary data inform about Science’s Faculties destroyed. A Chemistry Faculty was burned entirely, in a city very close to the epicenter of the earthquake. Here, in Santiago, we have several damages in laboratories from many research centers and universities. My lab was full of water the morning after the earthquake. A big amount of data was almost lost. Fortunately, equipment was unharmed. Some damages in structures and walls is also observed, but maybe they can be repaired in a few weeks. In other laboratories, where some of my friends are pursuing their Ph.D. research projects, the damages are more extensive, with chemical emergencies, equipment lost, structural damage…

Conicyt, the Government agency funding science, already declared a flexibility in some deadlines for applications and submission of results from research projects. We still don’t have news from other laboratories and research facilities in the areas more affected by the earthquake. The hope and faith that we all have is not only for science. It is also for the entire Chile.

Soon more news and photos.


Hi! I just wanted to post a little notice: I have my PhD Research Project exam this month. So, I will be off-air until then. I am very stressed and I just want to approve this exam very soon.

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