Pesticide levels considered environmentally friendly in Europe and Australia are, in fact, having a devastating effect on invertebrate insect biodiversity in nearby creeks and streams, a new study has found, showing the need for an urgent overhaul of the way pesticide risk is assessed. Water-dwelling invertebrates like worms, snails, crustaceans, mites and insects play a crucial role in regional ecosystems because they provide food for fish, birds and platypuses.

The study, published in Proceedings of the National Academy of Sciences (PNAS), found that invertebrate biodiversity, mostly insects, was slashed by up to 42% in the streams studied. The international research team, which included scientists from the University of Technology, Sydney, examined data on levels of pesticide toxicity in 48 and 24 sampling sites in Europe and Southern Victoria respectively.

The researchers selected creaks and streams that were close to crops of grape vines, orchards, berries, vegetables, corn, sugar beet or oil-seed. The sites selected had no wastewater treatment plants, industrial facilities, or mining drainage upstream, allowing the researchers to rule out the possibility that pollution was from non-agricultural sources.

“Current use pesticides in southern Victoria and regions in Germany and France is reducing the number of different types of animals without backbones, or invertebrates, living in streams and rivers. The animals most affected were mayflies, stoneflies, caddisflies and dragon flies,” said ecotoxicologist and aquatic ecologist from the University of Technoligy, Sydney, Dr Ben Kefford, who co-authored the paper. “Importantly, the reduction in the number of different types of invertebrates occurred at the regional scale.”

Pesticide regulation

The findings also show that pesticide regulation in Australia and Europe may be flawed. Pesticide regulation is intended to prevent threats to biodiversity or collateral elimination of insects that are not pests. “The regulation in both these continents is probably failing because they are both based on determining the effect of pesticides in the laboratory […] without studying the effects pesticides have in real streams and rivers,” Dr Kefford said.

Dr Jon Brodie, Senior Principal Research Officer at James Cook University, who was not involved in the study, said the findings did not surprise him. “We already know the current pesticide regulatory regime in Australia, at least, is not up to the mark for protecting aquatic biodiversity.”

Dr Brodie said that the results highlight a need for better pesticide use evaluation.  “The results could be used to show the inadequacy of the current protection regime and to improve it by doing more sophisticated analysis and addressing the cumulative nature of pesticide exposure,” he said.

Crop protection

Dr Richard Roush, Dean of Melbourne School of Land and Environment at the University of Melbourne, said the new findings were unsurprising. “I don’t think this paper makes a particularly strong case that the risk assessment needs to be across regional scales. To be used in practice, the new standards and methods in risk assessment do need to measure risk at biologically relevant concentrations and identify the specific pesticides that need to be better regulated, which are likely to be the insecticides rather than some of the other pesticides listed,” said Dr Roush, who was not involved in the study. “Before this is somewhat underway, the immediate implications for aquatic biodiversity are limited, because there is still huge demand for crop protection.”

However, Dr Kefford, who co-authored the paper, said that while pesticides were often regulated at a national level, the risk is mostly assessed by its effect on individual organisms rather than on real ecosystems. “Indeed, if pesticides kills some aquatic invertebrates it is not a major environmental problem but it is if it reduces biodiversity across a region,” he said.

“What is undeniable is the need for regulation to consider the effects of pesticides in real ecosystems and not be confined to effects in the laboratory and semi-natural ecosystems.”

This  article was originally published at The Conversation, by Michelle See-Tho

References:
Beketov, M., Kefford, B., Schafer, R., & Liess, M. (2013). Pesticides reduce regional biodiversity of stream invertebrates Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1305618110

Archaeopteryx’s claim to fame is that of the first true bird in the fossil record. It was the first dinosaur known to be able to fly, and it lived during the Jurassic, roughly 150 million years ago. It also helps to link birds to the dinosaur line itself, more specifically to a family of dinosaurs called Theropods (Greek for ‘beast-like foot’, due to their feet looking like the feet of predators).

First feathers
It begins in 1999, from China, with the discovery of Sinornithosaurus , a member of the Dromaeosaur line of theropod dinosaurs –  better known to most people as Raptors (after Velociraptor).

Since then, a bunch of other, new, raptor fossils have popped up also showing evidence of having borne feathers. Most notably Microraptor and Velociraptor. Though not all raptor species have been proven to have worn a coat of feathers, many of the raptors found so far that were originally thought to be without feathers have now been shown otherwise. Thus, it is now speculated by palaeontologists that the entire raptor line could have been feathered, including the big-and-bad Utahraptor .

But wait, it gets even fluffier…

In 2009, a feathered theropod named Anchiornis was found in China. Anatomy places the little guy in the same line as Troodon, another theropod originally thought not to possess feathers.

Fun fact: Troodon (pictured on the right) has been called the smartest of the dinosaurs, with an intelligence thought to equal that of your common chicken.

While it’s still not proven yet whether Troodon itself possessed feathers, it is in the same line as Anchiornis, and so some palaeontologists also depict Troodon with feathers.

Now for the grand finale:
Two other dinosaur fossils were found in China that belonged to a rather infamous line of theropods.

They are Dilong  and Guanlong , and both of them were feathered precursors to… Tyrannosaurus Rex.

Think about that for a moment: T-rex, with feathers.

No need for T-rex to worry yet, as no such feathery evidence has thus far been found. However, as with the raptor and troodon lines, the tyrannosaur line is populated with feathered, Jurassic ancestors to the more well-known, Cretaceous descendants. Palaeontologists, nonetheless, now think that it was likely that Tyrannosaurus young were feathered, with those feathers being lost as they grew into adulthood.

No need for dinosaurs in general to worry yet, either, as all the current feathered finds are of theropods only. I’m sure some people can rest easier on that fact.

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Justin Beckerman, an 18-year-old student and inventor from New Jersey, has made a submarine that can dive to 30 feet below the water’s surface. Check out this video to see how it did it, and how the submersible works.

Source: NJ.com, JustinBeckerman.com

Photo: JustinBeckerman.com

Antelope Canyon, Arizona, U.S.

Cappadocia, Anatolia, Turkey

‘Door to Hell’ , Derweze, Turkmenistan

Dragon’s blood trees, Socotra, Yemen

Giant Buddha, Leshan, China

Grand Prismatic Spring, Yellowstone National Park, U.S.

Hitachi Seaside Park, Hitachinaka, Japan

Odle Mountains, Italy

Red beach, Panjin, China

Rice terraces, Bali, Indonesia

Salar de Uyuni, Bolivia

The Wave, Arizona, U.S.

Sossusvlei, Namibia

Travertines, Pamukkale, Turkey

Tunnel of Love, Klevan, Ukraine

Giant’s Causeway, Antrim, Northern Ireland, U.K.

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For half the population, it comes three to five days each month, 12 months each year, for 40 years of our lives. Menstruation can be debilitating, relieving, disappointing, or simply an inconvenient fact of life.

But why do humans menstruate, when most animals don’t? When you shake the tree of life, you find that only a handful of mammals aside from us – primates, a small number of bat species, and the elephant shrew – have opted for the monthly bleed.

Each month the uterus prepares a thick and luxurious lining in preparation for the arrival of a fertilised egg – an embryo that will develop into a fetus and after nine months, a full-term baby. If no embryo arrives, there will be no pregnancy and menstruation sheds the thickened lining.

Evolution is often viewed in terms of a cost-benefit ledger: if something is costly, it must have some benefit. Women lose over half a standard glass of wine’s worth in iron-rich blood and tissue – about 90 millilitres – each time they menstruate, so the process does seem quite costly. And in the predator-filled environs of our early ancestors, leaving a trail of blood was presumably not advantageous.

So how did menstruation arise? Over recent decades, evolutionary biologists have come up with three key theories to explain human menstruation.

Cleansing mechanism

One controversial theory, proposed in the 1990s by self-taught biologist Margie Profet, suggested menstruation was a cleansing mechanism. Being the amorous species that we are, human females require a mechanism to regularly flush out the infection-laden sperm that gathers from our sexual conquests.

This argument was soon found to have more than a few flaws. For a start, women are more susceptible, not less, to infections such as chlamydia and gonorrhoea during menstruation, as the cervical mucus thins out.

The iron-rich blood also serves as an attractive food source for Staphylococcus aureus, of tampon-associated toxic shock syndrome notoriety.

And there is no correlation between level of promiscuity in us and our close primate relatives and heaviness of bleeding, as the theory predicts.

Invasive embryos

A more plausible explanation for menstruation is that it evolved to accommodate the peculiar way in which human embryos embed into the lining of the uterus – the endometrium – during pregnancy.

In some mammals with a placenta, a fertilised embryo attaches to the endometrium only superficially. In humans and other menstruating species, implantation is deep and invasive, and requires an especially luxurious lining to develop in preparation for implantation.

While other mammals are able to reabsorb the lining that adorns their fertile womb, the volume of tissue in humans is too great, so if no pregnancy ensues, it is expelled instead.

In the evolutionary cost-benefit analysis, building up the lining only when a pregnancy is on the cards – only when we ovulate once a month – could be less costly than maintaining this expensive lining indefinitely.

Another key difference between menstruators and non-menstruators is in the impetus for uterine thickening. In non-menstruating mammals, the final thickening of the endometrium (a process called decidualisation) only occurs once the lining senses the bleating signals from the embryo saying, “I’m here, now make my bed!”

Somewhere along the human evolutionary path, the dialogue between embryo and uterus shifted, so that the signals causing the endometrium to thicken came not from the embryo, but from the mother herself. Instead of being linked to the presence of the embryo, uterine thickening became linked to ovulation and the choreographed hormonal up-and-down that each woman cycles through on a monthly basis.

Maternal self-defence

But what’s with all this pre-emptive pampering? Not all mammals prepare for pregnancy so hopefully each month. Rabbits, for example, only ovulate and thicken their endometrium when they copulate.

American evolutionary biologists Deena Emera, Roberto Romero and Günter Wagner argue that the spontaneous thickening of the uterine lining is in fact a defence mechanism. Except the defence is against our own parasitic offspring, rather than sperm-borne infection.

Since mother and child do not share identical genes, their purposes are at odds. From the embryo’s perspective, the maximum benefit is gained from squeezing as many resources from its mother as possible. It even dampens its mother’s response to insulin, ensuring that a greater slice of the circulating sugar pie is placenta-bound during its nine-month residence.

The embryo tries to squeeze as many resources from its mother as possible. Image from shutterstock.com

The mother, meanwhile, prefers to be frugal with her resources, so that she can survive this pregnancy and go on to populate the next generation with additional children endowed with her unique genetic contribution.

There are two reasons that this maternal–fetal tug of war could have resulted in spontaneous thickening of the uterus. First, with implantation already invasive in humans and other menstruating species, the pre-thickened lining could be an evolutionary push-back to prevent the embryo from burrowing even deeper into the uterine wall.

The second reason is to protect the mother from expending valuable resources on faulty fetuses. The thickened lining could be an efficient way to sense – and if necessary, jettison – any tainted, and therefore unwanted, embryos. Around 30% to 60% of all human embryos are unceremoniously discarded in this way, before any signs of pregnancy occur.

While its evolutionary origins are firmly rooted in what takes place during pregnancy, the reality is that for most menstrual cycles, no embryo arrives. The decidual cells that have thickened the uterine lining pack up shop, the extracellular matrix keeping them all together breaks down, and the lining becomes as deciduous as the autumn leaves.

For Western most women who bear few children, this menstrual cycle is repeated 450 to 480 times over.

References:

Emera, D., Romero, R., & Wagner, G. (2012). The evolution of menstruation: A new model for genetic assimilation BioEssays, 34 (1), 26-35 DOI: 10.1002/bies.201100099

Blanks, A., & Brosens, J. (2013). Meaningful menstruation BioEssays, 35 (5), 412-412 DOI: 10.1002/bies.201300022

This original article was published by Dyani Lewis at The Conversation.

female menstrual cycle,menstruation research,cause of menstruation

In my mind, pills are like apps. Do you have a common problem to solve? There’s an app for that, as Apple has trademarked. Do you have some health related issue? There’s probably a pill for that. Blood pressure? Check. Cholesterol? Check. Social anxiety? Check. Erectile dysfunction? Check. Obesity? Check. Female libido? Oops! No check! But just wait! Big Pharma is working on that! As far back as January 2005, as published in the British Medical Journal, attempts have been made to develop a misnamed female Viagra.

But let’s go back to the beginning. Hypoactive sexual desire disorder. HSDD. It’s a lack or loss of sex drive (libido) in women that leads to distress. It’s not the same as erectile dysfunction in men which is more of a plumbing issue. Men can be troubled by ED and still be interested in sex. It’s the loss of interest leading to distress that drives the definition of HSDD. Obviously (or maybe not), it’s a complicated issue.

You’re not going to be interested in having sexual relations without your partner if you’re upset with him or her. You’re also not going to be interested in sexual relations if you’re tired from work (whether inside or outside the home), if you’re worried about money or your job, if you’re distracted by family and friends, etc. You’re also not going to be interested in sex if you’re depressed or taking certain medications of if you don’t have a positive self-image.

But what if it’s none of the above? That’s where Big Pharma has been trying but without much success to find an easy to take, side effect free solution to this relatively common situation in women. This post isn’t necessarily about the medicalization of the human condition (often referred to as disease mongering) but rather about the latest and greatest pill yet, Lybrido. You know it’s a big deal when Popular Science does a write up on a yet to be approved drug. And as expected, the New York Times also developed a nice review of the topic. But it took a bit more digging around to figure out just what’s in Lybrido: testosterone + sildenafil (the active ingredient in Viagra), as noted in the Neurocritic, a blogpost. So if you can’t wait for the science to catch up with good solid evidence and proof, ask your doc for the individual medications and play mad scientist.

References:
Moynihan, R. (2005). The marketing of a disease: female sexual dysfunction BMJ, 330 (7484), 192-194 DOI: 10.1136/bmj.330.7484.192

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You see them in sunflowers and artichokes. The familiar, concentric spiral-shaped Fibonacci sequence is part of a lot of flowering plants. These patterns precisely follow the Fibonacci sequence (1, 1, 2, 3, 5, 8), in which each digit (once you move along) is the sum of the previous two. But until now, nobody really knew how plants knew to make these mathematically precise patterns.

Researchers did know that the Fibonacci sequence provides one of the best ways for plants to maximize exposure for sunlight and other nutrients—seeds and flower steps are packed in the most efficient way possible. But scientists at the University of Arizona discovered, at least among sunflowers, that a plan growth hormone called auxin is responsible for creating the Fibonacci spirals.

Matthew Pennypacker and Alan Newell reported in Physical Review Letters that as sunflowers grow, their seeds in the head of the flower align themselves in annuli, which are closely arranged as the familiar spirals. The annuli shrink as the plant head grows and the spiral is formed. What’s causing the pattern? The researchers found that concentrations of auxin were highest right where seeds were about to be formed. So it was the auxin that led the spiral pattern formation. The researchers used a computer model that accurately predicted where auxin concentrations were going to be greatest—and how the patterns were formed.

Auxins were the first plant hormone to be discovered, and are involved in transforming stem cells into mature cells, as well as guiding the cell elongation process in plants. Since auxins are found in a wide variety of plants, the research suggests that these and other mathematical formulas may be behind many other plant growth patterns.

Source: ScienceNOW, Physical Review Letters

Photo: Wikimedia Commons

Pennybacker, M., & Newell, A. (2013). Phyllotaxis, Pushed Pattern-Forming Fronts, and Optimal Packing Physical Review Letters, 110 (24) DOI: 10.1103/PhysRevLett.110.248104

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Dogs have been at humankind’s side for thousands of years; we’ve bred them for size, ferocity, hunting assistance (actually, assistance of all kinds), and perhaps above all, companionship. Now, a number of studies show how dogs evolved from their wild wolf ancestors, and what all that breeding has led to.

A study led by researchers at Uppsala University of Sweden reported in Nature that dogs evolved from wolf ancestors by adopting a diet heavier on starches and other carbohydrates. By conducting next-generation whole-genome sequencing on both dogs and wolves, the researchers found a number of genes in dogs that differed from wolves. These genes were involved in various behaviors, and a significant set of genes controlled starch digestion and fat metabolism.

Thus, the dog evolved on its stomach. Literally. The Uppsala researchers believe that dogs branched out from wolves because they were adopting a diet heavier on starches, while wolves continued their mainly meat-based diet. Why did the dogs switch meals? At the time, human societies were becoming more farm-based, and our diets were also switching to heavier emphasis on grains. In addition, food was either stored or discarded, which made it much easier to procure than hunting. So, feeding a dog a heavy meat diet isn’t necessarily healthy.

Some researchers aren’t so sure that dog evolution is based entirely on diet. Greger Larson, a geneticist at Durham University in the UK, and Robert Wayne, a geneticist at UCLA, both think that saying dogs’ diets triggered evolution isn’t right. They think that other behavioral traits, such as linking up with human companions, may have played a stronger role. After all, the Uppsala team did find a number of behavior genes that diverged.

Since that evolutionary leap, however, we’ve been breeding dogs for all sorts of traits and tasks. But has all that breeding been healthy for dogs? Can breeding go too far?

One popular notion is that purebred dogs aren’t as healthy as the basic “mutt:” a dog that’s the mix of a number of breeds. A study of 90,000 purebred dogs and mongrels by the University of Calfornia, Davis, found, well, a mixed bag. While some conditions appear in purebreds, others are just as prevalent in mutts.

The UC Davis researchers discovered about 25,000 dogs that had at least one genetic disorder. When they compared disorders between mixed- and pure breeds, they found 13 disorders—cancers, adrenal gland disease and hip dysplasia—were common to both. Purebred dogs were more likely to have 10 disorders, including cardiomyopathy, elbow dysplasia and cataracts. One disease was particular to mutts—a specific type of knee injury. The data also showed one cause of death that affected mutts more than other breeds: being hit by an automobile.

The researchers saw patterns that suggested that dog breeds that are more recent or were bred from known lines (a practice that can preserve pathogenic mutations) were more likely to suffer from disorders that were known among purebred dogs. Meanwhile if a mutt had a genetic disorder, it was more likely from something that affects all dog breeds, regardless of lineage.

And they’ve all evolved to eat the same food.

Sources: Los Angeles Times, Nature

Bellumori TP, Famula TR, Bannasch DL, Belanger JM, & Oberbauer AM (2013). Prevalence of inherited disorders among mixed-breed and purebred dogs: 27,254 cases (1995-2010). Journal of the American Veterinary Medical Association, 242 (11), 1549-55 PMID: 23683021

Axelsson E, Ratnakumar A, Arendt ML, Maqbool K, Webster MT, Perloski M, Liberg O, Arnemo JM, Hedhammar A, & Lindblad-Toh K (2013). The genomic signature of dog domestication reveals adaptation to a starch-rich diet. Nature, 495 (7441), 360-4 PMID: 23354050

Short bouts of intermittent exercise throughout the day may be better than one vigorous workout in convincing your brain that you are full, according to a new study published in the journal Obesity.

The researchers, from the United States and Murdoch University, set out to find how the appetite-regulating hormone Peptide YY (PYY) fluctuates with intermittent or continuous exercise. The research team asked the 11 participants to do no exercise on day one, to do a one-hour morning exercise session on day two, and to do 12 five-minute bouts of exercise throughout the third day day. Blood was drawn every 15 minutes to assess hormones and the subjects were asked to rate their levels of hunger.

The researchers didn’t note any difference in PYY levels when comparing the two forms of exercise. But on the day the participants did shorter bursts of exercise more regularly, they reported feeling up to 32% fuller between 1pm and 3pm. They also felt fuller between 3pm and 5pm.

Study co-author Tim Fairchild, from Murdoch University’s School of Psychology and Exercise, said a regime of shorter exercise sessions presented a promising alternative for weight maintenance and weight loss.“Staying physically active at work and home is critical for maintaining low levels of hunger,” he said.

But it’s not just a matter of standing up a few more times at work. “You do actually have to go for a fairly hard five minute walk in order to see any benefits,” Dr Fairchild said.

Associate Professor Tim Crowe, from Deakin University, said the research built on existing evidence that people felt hungry after exercise, which could cause them to eat more. “But the overall benefit of exercise in helping with weight loss clearly puts it on the right side of the ledger,” said Professor Crowe, who was not involved in the study.

“The key message though is that Australians are nowhere near active enough, and for someone trying to keep their weight in check, then at least 60 minutes a day of physical activity is needed. “For busy people, this latest research shows that getting your ‘dose’ of exercise in many small five or ten minute chunks all throughout the day could be just as effective as sweating it out at the gym.”

David Dunstan said the next step was to work out how the finding translated to people’s working lives. The researchers “used a more moderate intensity type approach, that’s where some people may start sweating while they’re exercising,” he said. “But what happens when you start scaling this down to what is practical and meaningful? You could go and walk the stairs but you’re going to be in your work clothes,” he said.

“So what can people fit into their daily lives without too much disruption to their productivity?” Professor of Medicine at the University of Melbourne, Joseph Proietto, said the study was well designed but with just 11 participants, the numbers were small. “It would be useful if someone would undertake a repeat study with more subjects,” he said. Professor Proietto said that although the researchers examined PYY, there were many other hormones that could also affect appetite, including ghrelin (which stimulates hunger) and insulin.

This article was originally published by Fron Jackson-Webb, at The Conversation.

References:
Holmstrup, M., Fairchild, T., Keslacy, S., Weinstock, R., & Kanaley, J. (2013). Satiety, but not total PYY, is increased with continuous and intermittent exercise Obesity DOI: 10.1002/oby.20335

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