ISEMPH Early Bird Deadline April 14th!

ISEMPH Early Bird Deadline April 14th!

April 14 is the last day for reduced fee registration for the August 2017 Meeting of the International Society for Evolution, Medicine and Public Health in Groningen, Netherlands. ISEMPH members get a special further reduced rate, and those who also register for the coordinated meeting of the European Society for Evolutionary Biology get 20% off both meetings.
The full program of more than 100 presentations is now available at the website. 

Click here to register now while fees are low!  

 

How a beneficial gut microbe adapted to breast milk

How a beneficial gut microbe adapted to breast milk

It is now well documented that the best way for an infant’s gut (largely sterile at birth) to get populated by the bacterial components of a healthy microbiota is through its mother’s milk. Over 700 species of bacteria have been found in breast milk including the prominent probiotics Lactococcus, Leuconstoc and Bifidobacterium. In “Body by Darwin” I described an extraordinary evolved symbiosis between Bifidobacterium longum and humans whereby human mothers express large quantities of complex long-chain sugars called oligosaccharides in breast milk even though their babies cannot digest them – they completely lack the enzymes to do the job. It turns out that the oligosaccharides are never meant for the baby – but to allow Bifidobacteria a competitive edge in the large intestine. B. longum, for instance, has a suite of 700 unique genes that allow it to digest oligosaccharides such that breast-fed babies become the perfect ecological niche for this bacterium. Now a group of scientists from Japan have added the enzymatic specifics to this story. They have shown that the two main species of Bifidobacterium – longum and bifidum – have evolved different ways to crack open specific oligosaccharides. Bifidobacterium bifidum, they say, possesses a glycoside hydrolase family 20 lacto-N-biosidase for liberating lacto-N-biose I from lacto-N-tetraose, an abundant oligosaccharide unique to human milk, while Bifidobacterium longum subsp. longum has a non-classified enzyme (LnbX), thanks to molecular evolution from the former enzyme, to exploit the same sugar. By determining the crystal structure of the catalytic domain of LnbX they provide evidence for the creation of a novel glycoside hydrolase family, GH136, and show that it is indispensable for B. longum growth on lacto-N-tetraose and is therefore a key genetic factor for persistence in the gut of breast-fed infants. Their results, they say, suggest that human milk oligosaccharides have been the main selective pressure for the evolution of the gene lnbX in B. longum, because a stronger correlation between the gene and bacterial persistence was detected in the stools of breast-fed infants than in those of mixed-fed infants. It seems likely that a whole range of bifidobacterial species and subspecies employ different strategies, involving the evolution of a family of enzymatic complexes, to exploit lacto-N-tetraose, so that this oligosaccharide can be shared among members of the genus and even among strains belonging to the same species/subspecies, but withheld from other bacterial species. it is a wonderful example of the evolution of a complex gut ecosystem of various bifidobacteria which avoids competition for a strategic sugar, to which they all have exclusive access, all of which has been driven by the complexity of mother’s milk.

Why resistance develops to antibiotics but not vaccines

Why resistance develops to antibiotics but not vaccines

David Kennedy and Andrew Read have kindly supplied the following teaser for their latest paper in Proceedings Of The Royal Society B. As they point out, this “armchair speculation” has elicited a gamut of reactions ranging from awe to scorn and so we are sure they would welcome commentary on this paper from the readers of Evmedreview!

Andrew Read

Dave Kennedy and Andrew Read

Center for Infectious Disease Dynamics, Departments of Biology and Entomolology, Penn State

David Kennedy

Evolution is perhaps the world’s greatest problem solver. It has found innumerable solutions to blistering environmental insults. Nowhere is this clearer than for drug resistance. Pathogen evolution has undermined virtually every known chemotherapeutic drug. Yet rubbing a cowpox pustule into a person’s open wound somehow confounded evolution. Most modern vaccines have done so too: they work as well as they did when they were first introduced. Why can evolution rescue pathogens from drugs but not from vaccines?

When we first discussed this question, we were surprised not to agree on an answer. It seemed that any of a laundry list of features might help explain why vaccines are more evolution-proof than drugs. We were also surprised to find barely any discussion of the problem in the literature. A few people had asked why resistance to measles or smallpox vaccines failed to evolve, but the answers were specific to those viruses. What was the general answer?

We disagreed for months before one of us (DK) persuaded the other (AR) that, ironically, the most plausible answer lay in processes well known in agricultural resistance management. This solution—which we just published after a grueling time with reviewers—is essentially armchair speculation. We cannot yet know whether it is correct. Reactions from colleagues have ranged from ‘that is obvious’ to ‘that is wrong’ and have involved adjectives like ‘superficial’ and ‘stimulating’, as well as the opinion that our article reads like an undergraduate essay. We hope that the simplicity of our argument breeds the kind of skepticism that leads to new data and new theories. The problem seems important. Will next-generation vaccines fail? Can drugs be made as evolution-proof as vaccines? Which cancer therapies have the greatest potential to work?

New book: Biochemical Adaptation–Make Biochemistry interesting and sensible

New book: Biochemical Adaptation–Make Biochemistry interesting and sensible

Just out from Sinauer, a new version of the classic text

Biochemical Adaptation 1st Edition
by George N. Somero, Brent L. Lockwood, Lars Tomanek

If only medical students could learn their biochemistry from this book!  So many wonderful examples.

From the Publisher’s Web Page: The abiotic characteristics of the environment—including temperature, oxygen availability, salinity, and hydrostatic pressure—present challenges to all biochemical structures and processes. This volume first examines the nature of these perturbations to biochemical systems and then elucidates the major adaptive strategies that enable organisms from all Domains of Life—Archaea, Bacteria, and Eukarya—to conserve common types of biochemical structures and processes across a wide range of environments. In addition to these conservative adaptations that foster a biochemical unity among diverse species, other adaptations can be viewed as innovative changes that enable organisms to exploit new features of the environment that may themselves be the result of biological activities.

The opening chapter outlines the basic principles of biochemical adaptations and raises the questions that serve as the focal points for the detailed analysis found in the next three chapters, which are devoted to the study of relationships involving oxygen, temperature, and water-solute effects. In these three chapters, the effects of the variable in question on fundamental biochemical processes and structures are examined. This analysis forms a basis for the subsequent analysis of how adaptive changes modify biochemical systems to establish environmental optima and tolerance limits. This analysis includes examples from all Domains of Life to emphasize the commonality of the fundamental strategies of biochemical adaptation.

The final chapter examines the challenges organisms face from the rapid environmental changes that are occurring in the Anthropocene. The effects of co-occurring changes in multiple stressors are examined to provide a realistic and integrative analysis of effects of global change. The underlying genetic capacities of different types of organisms to adapt to rapid environmental change are discussed to provide a basis for predicting the relative success different species—including our own—face in a rapidly changing world.

Genetic diversity: Driving cancer evolution

Genetic diversity: Driving cancer evolution

There are two related and interesting articles on cancer evolution in a recent edition of eLife. The first is a commentary by Devon M Fitzgerald and Susan M Rosenberg, of the Baylor College of Medicine, on a paper in the same issue  titled “TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24− cancer cells.” As Fitzgerald and Rosenberg explain, mutations don’t always arise randomly at uniform rates. Many cells and organisms have been shown to increase mutagenesis in response to stress. In the case of cancer this could come about through the insult to cancer cells of anti-cancer medication. The paper by Raffaella Sordella, and her colleagues, of Cold Spring Harbor Laboratory documents a good example of this by showing that TGF-beta signaling can temporarily reduce the fidelity of DNA repair leading to genetic diversity in progeny cells. This can result in the evolution of resistance to chemotherapy.

The CSHL team concentrated on CD44+/CD24− cells which arise in cancer cell lines and behave like stem cells in reaction to the TGF-beta signaling pathway so that they become continuously active. These cells are linked to drug-resistance, metastasis and other poor outcomes for patients, they say. The faulty DNA repair causes copy number changes to genes – a well recognised hall-mark of cancer evolution. They also showed that the gene PMS1 – which is important for so-called mismatch-repair of DNA was also less active in CD44+/CD24− cells. Mismatch repair corrects small errors in DNA replication, and so errors here can allow thousands of small point mutations to pile up in cancer cells.

All this, say Fitzgerald and Rosenberg, points to the importance of looking for “anti-evolvability” drugs rather than drugs which try to deal with the outcomes of cancer evolution. By inhibiting evolution you could, theoretically, decrease the chances of the evolution of resistance.

Is atherosclerosis a modern disease after all?

Is atherosclerosis a modern disease after all?

What factors should we blame most for the continuing pandemic of heart and artery disease throughout the Western world? The argument has endured more twists and turns than California Route 1. For years, the diet cholesterol hypothesis has held sway, with added blame attached to smoking and a couch potato lifestyle. Before the ascendency of the cholesterol hypothesis, cardiology favored inflammation as the main driving force for atherosclerosis, and interest in inflammation has returned thanks to studies suggesting C-reactive protein is a much better indicator of heart problems lying in wait for asymptomatic individuals than cholesterol levels or high blood pressure; a meta-analysis showing that dietary change has no impact on the risk of a heart attack; studies showing that atherogenic processes in arterial walls are driven by the immune system; and paleocardiology studies showing that pre-industrial and prehistoric societies had high levels of arterial plaque despite high exercise levels and a frugal diet low in saturated fat. i.e. that susceptibility to heart disease is not a modern phenomenon. Now, a study published last Friday in The Lancet, based on measurements taken from members of the Tsimane – a forager-horticulturalist population living in the Bolivian Amazon basin – dramatically switches the argument back again. The Tsimane have extraordinarily low rates of coronary artery disease, low blood pressure, low blood glucose, and low “bad” cholesterol (LDL), despite enduring chronic high levels of systemic inflammation due to the high pathogenic load they carry. It is infection that carries them off – not heart disease.

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