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The first issue of Evolution, Medicine, and Public Health has been published.   The journal is edited by Stephen Stearns and published by the Oxford University Press.    The Table of Contents is below.  All articles are Open Access.

Editorial  by Stephen C. Stearns

EMPH (2013) 2013: 1-2 doi:10.1093/emph/eos001

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Original Research Articles Continue Reading »

Her article is in the current issue of The Chronicle Review.

Article begins: The first thing you have to do to study 4,000-year-old DNA is take off your clothes.  I am standing with Oddný Ósk Sverrisdóttir in the airlock room next to the ancient-DNA laboratory at Uppsala University, in Sweden, preparing to see how she and her colleagues examine the bones of human beings and the animals they domesticated thousands of years ago. These scientists are looking for signs of changes in the genes that allow us to consume dairy products past the age of weaning,  Read more 

 

Smith, H. F., Parker, W., Kotzé, S. H., & Laurin, M.

Multiple independent appearances of the cecal appendix in mammalian evolution and an investigation of related ecological and anatomical factors.

Comptes Rendus Palevol(0). doi: http://dx.doi.org/10.1016/j.crpv.2012.12.001 (not open access)

Abstract:  Although the cecal appendix has been widely viewed as a vestige with no known function or a remnant of a formerly utilized digestive organ, the evolutionary history of this anatomical structure is currently unresolved. A database was compiled for 361 mammalian species, and appendix characters were mapped onto a consensus phylogeny along with other gastrointestinal and behavioral characters. No correlation was found between appearance of an appendix and evolutionary changes in diet, fermentation strategy, coprophagia, social group size, activity pattern, cecal shape, or colonic separation mechanism. Appendix presence and size are positively correlated with cecum and colon size, even though this relationship rests largely on the larger size of cecum and colon in taxa that have an appendix. The appendix has evolved minimally 32 times, but was lost fewer than seven times, Continue Reading »

The Polycystic Ovary Syndrome and recent human evolution
By Corbett SMorin-Papunen L.
Mol Cell Endocrinol. 2013 Jan 23. pii: S0303-7207(13)00004-X. doi: 10.1016/j.mce.2013.01.001. (not open access)

Abstract: The Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder characterised both by reproductive and metabolic disturbance, and is the most common cause globally of ovarian infertility. It is also a familial polygenic condition, linked genetically to both Type 2 diabetes and the metabolic syndrome. The striking evolutionary paradox of this prominent genetically-based condition, which impairs fertility, is that not only should it have diminished in prevalence, but it should have done so rapidly Continue Reading »

Toward a general evolutionary theory of oncogenesis (pages 70–81)

By Paul W. Ewald and Holly A. Swain Ewald

Evolutionary Applications   Special Issue: Cancer    Volume 6, Issue 1, pages 70–81, January 2013

Abstract: We propose an evolutionary framework, the barrier theory of cancer, which is based on the distinction between barriers to oncogenesis and restraints. Barriers are defined as mechanisms that prevent oncogenesis. Restraints, which are more numerous, inhibit but do not prevent oncogenesis. Continue Reading »

The new Journal of Evolutionary Medicine, edited by Paul Ewald, has published 5 articles since its initiation in late 2012.  See below for titles and links to open access articles.

Welcome to a New Journal——Journal of Evolutionary Medicine, Paul W. Ewald
Volume 1 (2012), Article ID Q120501, 1 Page   Published: May 2012
Continue Reading »

 The Jan 2013 Special Issue of Evolutionary Applications about cancer has two review articles on how evolutionary principles can advance cancer research.  They offer somewhat different, but complementary visions of how applications of principles from evoluitonary biology can  advance cancer research. They are open access and can be downloaded by clicking the titles below. Continue Reading »

 

Recently, a valued friend and scientific colleague of mine (Jonathan Yewdell of the NIAID in Bethesda) made me aware of a netcast (http://www.twiv.tv/) and associated blog (http://www.virology.ws/) relating to virology.  The originator of both is Vincent Racaniello, a well-known and highly regarded virologist and professor of microbiology at Columbia University.  Dr. Racaniello currently happens to be curating a survey (http://www.virology.ws/are-viruses-alive/) asking people to answer the question: “Are viruses living?” Continue Reading »

Evolutionary Applications, an open-access journal edited by Louis Bernatchez, has just published a special issue on cancer.     This is a milestone for evolutionary medicine, and perhaps for cancer research as well. The special issue, edited by  Frederic Thomas, Michael Hochberg, Athena Aktipis, Carlo Maley and Ursula Hibner, offers 14  articles. The first and last articles are broad reviews. The rest are on topics ranging from etiology, to tumor ecology, and new strategies for chemotherapy.    Together, they make it vividly clear that malignancies are products of somatic evolution in individual bodies that develop, or do not, because of how natural selection shaped traits that increase vulnerability, and capacities for resistance, in rapidly changing environments.  The Evolution and Medicine Review will feature several articles in coming days. In the meanwhile, see the Table of Contents below, with links to the full articles.  Continue Reading »

In 1996, Dean et al. (Science), demonstrated that a loss-of-function allele (CCR5Δ32) encoding a version of the chemokine receptor, CCR5, confers very substantial resistance to infection with HIV-1 in the homozygous state and slows progression in the heterozygous state.  Given the relatively recent origin of HIV-1, this finding raised the question of what source of selection could account for the frequency, approximately 0.08 among Caucasians according to Dean et al., of this allele.  A recent paper (Alonzo et al., 2013) offers new information on a relationship between CCR5 and a different pathogen that might offer insight into the evolutionary trajectory of CCR5Δ32.

The new study presents compelling evidence that leukotoxin ED (LukED), one of a family of bi-component exotoxins produced by Staphylococcus aureus, can bind to CCR5 and thereby cause cell death.  LukED consistently produces substantially more cytotoxicity for CCR5+ than CCR5- cell lines of several types.  Ligands for CCR5, including the drug, maraviroc, which is approved for clinical treatment of HIV-1 infection, significantly inhibit both the binding of LukED to cells and the magnitude of associated cytotoxicity.  LukED also binds to and kills CCR5+ primarycells, such as human memory T cells, macrophages, and dendritic cells. Continue Reading »

Last year, my colleagues and I published Nutrient Signaling: Evolutionary Origins of the Immune-Modulating Effects of Dietary Fat. We were prompted to write this paper because of several observations:

1) Chronic inflammatory diseases, such as obesity, diabetes, and atherosclerosis have reached epidemic proportions and account for growing proportion of global mortality and morbidity.

2) A growing body of evidence has shown that modern dietary habits - including overnutrition and exposure to certain nutrients and processed foods – contribute to chronic inflammatory diseases.

3) Nutrients have vastly differing effects on the immune system. Certain nutrients promote pro-inflammatory signaling and dangerous changes in metabolism; other nutrients reduce immune activation, have anti-inflammatory signaling properties, and protect against metabolic diseases. These observations raise the question, why?

Until recently, there has been no satisfactory explanation for these divergent immune and metabolic effects. In particular, Continue Reading »

Fecal Microbiota Transplantation — An Old Therapy Comes of Age

Ciarán P. Kelly, M.D. in this week’s New England Journal of Medicine

January 16, 2013DOI: 10.1056/NEJMe1214816  Open access

[Interestingly, neither this editorial summary nor the original research report (see below)  mention ecology or evolutionary biology.  They are presented as purely empirical studies without any foundation in theory]

In 1958, doctors in Denver administered feces by enema to their patients with fulminant, life-threatening pseudomembranous enterocolitis.1 The goal of this infusion of donor feces (also termed fecal microbiota transplantation [FMT]) was to “re-establish the balance of nature” within the intestinal flora to correct the disruption caused by antibiotic treatment. They reported “immediate and dramatic” responses and concluded that “this simple yet rational therapeutic method should be given more extensive clinical evaluation.” Continue Reading »

The origin of specificity by means of natural selection: evolved and nonhost resistance in host–pathogen interactions

By Janis Antonovics, Mike Boots, Dieter Ebert, Britt Koskella, Mary Poss, and Ben M. Sadd

Evolution   Volume 67, Issue 1, pages 1–9, January 2013  (open access)

 Abstract: Most species seem to be completely resistant to most pathogens and parasites. This resistance has been called “nonhost resistance” because it is exhibited by species that are considered not to be part of the normal host range of the pathogen. A conceptual model is presented suggesting that failure of infection on nonhosts may be an incidental by-product of pathogen evolution leading to specialization on their source hosts. This model is contrasted with resistance that results from hosts evolving to resist challenge by their pathogens, Continue Reading »

A major problem confronting physicians, nurses, and other hospital personnel is transmission of pathogens among inpatients or between medical personnel and inpatients (in either direction).  A crucial component in efforts to control such infectious outbreaks in hospital wards is determining whether particular cases are linked by instances of person-to-person transmission.  Standard methods of analysis involve epidemiological data, determinations of antibiotic sensitivities, and evaluation (multilocus sequence typing or MLST) of alleles at a limited number (<1%) of bacterial loci.  A recent paper by Harris et al. in Lancet Infect Dis. (2012) offers results that support the use of whole-genome sequencing (WGS), which covers >95% of loci, of infectious isolates from individuals that might reasonably be thought to be part of an outbreak.  In this particular study, focused on infection by methicillin-resistant Staphylococcus aureus (MRSA), both inpatients and outpatients were likely involved.

Continue Reading »

 By Beth Skwarecki Posted: November 29, 2012 in the PLoS Public Health Blog

You fill a prescription for antibiotics, and have 14 days worth of pills in your hand. Pop quiz: If you want to be a good citizen and prevent the spread of antibiotic resistance, how many of those pills should you take?

The sticker on the bottle is clear: all of them. In India, where Andrew Read studies infectious disease, resistance is so prevalent that standard malaria treatment includes not just the pills, but a boy who comes to your home each day to check that you’ve taken your dose. And yet, Read believes that aggressive treatment with antibiotics is increasing the spread of resistance, not controlling it.  To read the rest, click here

12  videos from the 2011 Evolution and Medicine Course at Mt. Desert Island are available online at the links here

 The videos from the 2012 course will hopefully be online soon.

Information on a possible 2013 course will be annouced on the Evolution and Medicine Review.

A new article in Evolutionary Applications by Hochberg, M. E., Thomas, F., Assenat, E., & Hibner, U. (2012).   doi: 10.1111/eva.12033  (open access)

Abstract:   Evolutionary theory predicts that once an individual reaches an age of sufficiently low Darwinian fitness, (s)he will have reduced chances of keeping cancerous lesions in check. While we clearly need to better understand the emergence of precursor states and early malignancies as well as their mitigation by the microenvironment and tissue architecture, we argue that lifestyle changes and preventive therapies based in an evolutionary framework, applied to identified high-risk populations before incipient neoplasms become clinically detectable and chemoresistant lineages emerge, Continue Reading »

A paper recently appearing in Science (Näsvall et al. 2012) offers a new insights into the mechanisms by which gene duplication can lead to new genes, gene products, and functions.  The new scheme is termed the innovation-amplification-divergence (IAD) model.  Continue Reading »

This week’s Nature has an open access Outlook section “Physical Scientists Take On Cancer.”
Two of the more intriguing articles turn out to be about evolutionary applications to cancer biology.
One is about mathematical modeling.  The other is a short Perspectives piece by Robert Gatenby, Finding Cancer’s First Principles.  The first paragraphs are below.

Robert Gatenby

Dazzling technological advances in molecular biology have transformed the biology of cancer and generated thousands of articles in the burgeoning fields of cancer genomics, proteomics, metabolomics and others. Yet researchers have revealed significant heterogeneity even between cancer cells in the same tumour, leading some to question the clinical value of this vast enterprise. Evolution can cause the genetic profiles in one region to be substantially different to those in distant or even adjacent sites — the conventional solution to this problem is greater investment in molecular technology so that entire cancer populations can be analysed cell by cell.

Now consider a different timeline. Suppose these technological developments had not occurred and we lacked the ability to obtain molecular data on any cancer population. Clearly, we would know less about cancer genetics, but would we also know less about cancer biology? I believe that the answer is “not necessarily”, and that we might actually know more.

Read the whole article here 

Therapeutic Helminth Infection of Macaques with Idiopathic Chronic Diarrhea Alters the Inflammatory Signature and Mucosal Microbiota of the Colon

By Broadhurst, MJ et al. in PLoS Pathogens, Nov 15, 2012  doi:10.1371/journal.ppat.1003000  (open access)

Only 5 subjects!  But dramatic results, nonetheless.

Author’s Summary> Young macaques kept in captivity at Primate Research Centers often develop chronic diarrhea, which is difficult to treat because it is poorly understood. This disease shares many features with ulcerative colitis, which is an autoimmune disease affecting the intestinal tract of humans. Recently, parasitic worms have been used in clinical trials to treat inflammatory bowel diseases in humans with positive results, but very little is known about how worms can improve symptoms. We performed a trial where we treated macaques suffering from chronic diarrhea with human whipworms, collecting gut biopsies before and after treatment. We found that 4 out of the 5 treated macaques improved their symptoms and studied the changes in their gut immune responses, as they got better. We found that after treatment with worms, the monkeys had less bacteria attached to their intestinal wall and a reduced inflammatory response to the gut bacteria. Additionally, the composition of gut bacteria was altered in the sick macaques and was restored close to normal after treatment with whipworms. These results provide a potential mechanism by which parasitic worms may improve the symptoms of intestinal inflammation, by reducing the immune response against intestinal bacteria.

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Thanks to Jeff Kopmanis at the University of Michigan for technical help that makes this publication possible.