What do Alzheimer’s disease, intestinal infarcts, supercentenarians, and some rare neurological diseases have in common?

by Kris Verburgh

Proteins!

Proteins are an important factor in aging. When we understand the role of proteins in the aging process, we can also figure out how we can slow it down—via our diet, among other things. Proteins consist of thousands of atoms. Proteins have different, specific shapes. It is the specific shape that determines the type of protein. The body contains more than 20,000 different kinds of proteins. Since proteins are clusters of atoms, and since atoms are minuscule in size, proteins are also very small. The average diameter of a protein is about 10 nanometers (a nanometer is one millionth of a millimeter).

Proteins have two functions: First, they are the building blocks of our cells. A cell contains millions of proteins that provide shape and structure to our cells. Just as wooden beams form the framework for a house, long rods of proteins form the specific shape of the cell. White blood cells can capture bacteria with their long, protruding arms because the arms contain a hinging framework of proteins that moves the arm of the white blood cell toward the bacteria. The cells that form our bronchia have long protrusions that wave back and forth to sweep up dust and mucus from the bronchia. The framework of these long protrusions is made up of proteins.

Second, proteins are also the workhorses of our cells. They perform almost all tasks in and around our cells: They break down substances such as drugs, alcohol, or food; they build up substances such as fats or hormones; they allow substances such as glucose or sodium to pass into and out of the cells; and they store or package other substances, like iron or vitamin B12. There is virtually nothing about our body that proteins are not involved in. Specific proteins in the cells of your stomach produce and secrete stomach acid. Other proteins located in the wall of nerve cells in your buttocks and back register pressure, which allows you to feel the chair in which you are sitting right now. Certain proteins in the cells of your eye register light, which allows you to read this book. Long protein strands in your muscles can shorten and contract them, so that you can turn over this page, but also dance, laugh, or walk. Proteins are the engines of life. The DNA in our cells contains the instructions for building proteins. Without proteins there is no life.

There is one more thing you need to know; namely, that proteins are made up of strands of amino acids. There are twenty types of amino acids in the human body (that can form proteins). Amino acids are small atom clusters that are always built according to a fixed plan. Amino acids are threaded like a pearl necklace to form a protein. This long strand of amino acids folds itself into a specific shape, such as a ball, a rod, or a hollow cylinder, forming a specific protein. This folding is possible because the atoms of which the strand is made are positively or negatively charged and can attract or repel one another.

The relationship between atoms, amino acids, and proteins can be pictured as follows. Just as there are various types of Lego blocks with different colors and sizes, there are also different atoms, for example hydrogen, oxygen, carbon, and so forth. Just as Lego blocks can build small basic structures, such as walls, windows, or roofs, atoms can build the twenty different amino acids. And just as these small basic Lego structures can build houses, amino acids can build proteins. A protein can consist of a few dozen of amino acids (a small house) or up to many thousands (a gigantic palace). Readers who want to learn more about proteins and amino acids can find more details at the end of the book, in the section “Additional Reading.”

Proteins, and therefore amino acids, are found primarily in meat. Meat consists mainly of muscle cells, which are full of proteins. Fish, eggs, and cheese also contain a lot of proteins; and the proteins we eat do not only come from animals —plants contain proteins as well. Rich sources of vegetable proteins are nuts, legumes, tofu, and certain vegetables, such as broccoli. As we will discuss later, vegetable proteins are healthier than animal proteins.

Copyright © 2015, 2018 by Kris Verburgh

Illustrations copyright © 2015 by CMRB, unless otherwise indicated Translation copyright © 2018 by The Experiment, LLC

How do avatars and simulation work?

by Scott Zimmer, JD

Principal terms

– Animation variables (avars): defined variables used in computer animation to control the movement of an animated figure or object.

– Keyframing: a part of the computer animation process that shows, usually in the form of a drawing, the position and appearance of an object at the beginning of a sequence and at the end.

– Modeling: reproducing real-world objects, people, or other elements via computer simulation.

– Render farm: a cluster of powerful computers that combine their efforts to render graphics for animation applications.

– Virtual reality: the use of technology to create a simulated world into which a user may be immersed through visual and auditory input.

 

Abstract

Avatars and simulation are elements of virtual reality (VR), which attempts to create immersive worlds for computer users to enter. Simulation is the method by which the real world is imitated or approximated by the images and sounds of a computer. An avatar is the personal manifestation of a particular person. Simulation and VR are used for many applications, from entertainment to business.

Virtual Worlds

Computer simulation and virtual reality (VR) have existed since the early 1960s. While simulation has been used in manufacturing since the 1980s, avatars and virtual worlds have yet to be widely embraced outside gaming and entertainment. VR uses computerized sounds, images, and even vibrations to model some or all of the sensory input that human beings constantly receive from their surroundings every day. Users can de ne the rules of how a VR world works in ways that are not possible in everyday life. In the real world, people cannot y, drink re, or punch through walls. In VR, however, all of these things are possible, because the rules are defined by human coders, and they can be changed or even deleted. This is why users’ avatars can appear in these virtual worlds as almost anything one can imagine—a loaf of bread, a sports car, or a penguin, for example. Many users of virtual worlds are drawn to them because of this type of freedom.

Because a VR simulation does not occur in physical space, people can “meet” regardless of how far apart they are in the real world. Thus, in a company that uses a simulated world for conducting its meetings, staff from Hong Kong and New York can both occupy the same VR room via their avatars. Such virtual meeting spaces allow users to convey nonverbal cues as well as speech. This allows for a greater degree of authenticity than in telephone conferencing.

Mechanics of Animation

The animation of avatars in computer simulations often requires more computing power than a single workstation can provide. Studios that produce animated films use render farms to create the smooth and sophisticated effects audiences expect.

Before the rendering stage, a great deal of effort goes into designing how an animated character or avatar will look, how it will move, and how its textures will behave during that movement. For example, a fur-covered avatar that moves swiftly outdoors in the wind should have a furry or hairy texture, with fibers that appear to blow in the wind. All of this must be designed and coordinated by computer animators. Typically, one of the first steps is keyframing, in which animators decide what the starting and ending positions and appearance of the animated object will be. Then they de- sign the movements between the beginning and end by assigning animation variables (avars) to different points on the object. This stage is called “in-betweening,” or “tweening.” Once avars are assigned, a computer algorithm can automatically change the avar values in coordination with one another. Alternatively, an animator can change “in-between” graphics by hand. When the program is run, the visual representation of the changing avars will appear as an animation.

In general, the more avars specified, the more detailed and realistic that animation will be in its movements. In an animated lm, the main characters often have hundreds of avars associated with them. For instance, the 1995 lm Toy Story used 712 avars for the cowboy Woody. This ensures that the characters’ actions are lifelike, since the audience will focus attention on them most of the time. Coding standards for normal expressions and motions have been developed based on muscle movements. The MPEG-4 international standard includes 86 face parameters and 196 body parameters for animating human and humanoid movements. These parameters are encoded into an animation le and can affect the bit rate (data encoded per second) or size of the le.

Educational Applications

Simulation has long been a useful method of training in various occupations. Pilots are trained in flight simulators, and driving simulators are used to prepare for licensing exams. Newer applications have included training teachers for the classroom and improving counseling in the military. VR holds the promise of making such vocational simulations much more realistic. As more computing power is added, simulated environments can include stimuli that better approximate the many distractions and de- tailed surroundings of the typical driving or flying situation, for instance.

Vr in 3-d

Most instances of VR that people have experienced so far have been two-dimensional (2-D), occurring on a computer or movie screen. While entertaining, such experiences do not really capture the concept of VR. Three-dimensional (3-D) VR headsets such as the Oculus Rift may one day facilitate more lifelike business meetings and product planning. They may also offer richer vocational simulations for military and emergency personnel, among others.

Bibliography

Chan, Melanie. Virtual Reality: Representations in Contemporary Media. New York: Bloomsbury, 2014. Print.

Gee, James Paul. Unified Discourse Analysis: Language, Reality, Virtual Worlds, and Video Games. New York: Routledge, 2015. Print.

Griffiths, Devin C. Virtual Ascendance: Video Games and the Remaking of Reality. Lanham: Rowman, 2013. Print.

Hart, Archibald D., and Sylvia Hart Frejd. The Digital Invasion: How Technology Is Shaping You and Your Relationships. Grand Rapids: Baker, 2013. Print.

Kizza, Joseph Migga. Ethical and Social Issues in the Information Age. 5th ed. London: Springer, 2013. Print.

Lien, Tracey. “Virtual Reality Isn’t Just for Video Games.” Los Angeles Times. Tribune, 8 Jan. 2015. Web. 23 Mar. 2016.

Parisi, Tony. Learning Virtual Reality: Developing Immersive Experiences and Applications for Desktop, Web, and Mobile. Sebastopol: O’Reilly, 2015. Print.

 

5 Reasons Why You Really Should Wear Gardening Gloves

Gardening is a great way to relax, be one with nature and get your hands dirty. But lurking in that pleasant environment are some nasty bacteria and fungi, with the potential to cause you serious harm. So we need to be vigilant with gardening gloves and other protective wear.
Soils contain all sorts of bacteria and fungi, most of which are beneficial and do helpful things like breaking down organic matter. But just as there are pathogenic bacteria that live on your body amid the useful ones, some microorganisms in soil can cause serious damage when given the opportunity to enter the body. This commonly happens through cuts, scrapes or splinters.
Plants, animal manure, and compost are also sources of bacteria and fungi that can cause infections.


1. Tetanus

Traditionally, the most common and well-known infection is tetanus, caused by Clostridium tetani, which lives in soil and manure. Infections occur through contamination of cuts and scrapes caused by things in contact with the soil, such as garden tools or rose thorns.
Fortunately, most people have been vaccinated against tetanus, which means even if you are infected, your body is able to fight back against the bacteria to prevent it becoming serious. Symptoms include weakness, stiffness and cramps, with the toxins released leading to muscular paralysis and difficulty chewing and swallowing – hence the common term for tetanus of lockjaw.


2. Sepsis

Bacteria such as Escherichia coli, Salmonella, Campylobacter jejuni, and Listeria monocytogenes are often present in gardens as a result of using cow, horse, chicken or other animal manure. Bacterial infections can lead to sepsis, where the bacteria enter the blood and rapidly grow, causing the body to respond with an inflammatory response that causes septic shock, organ failure, and, if not treated quickly enough, death.
A high-profile case recently occurred in England, where a 43-year-old solicitor and mother of two died five days after scratching her hand while gardening. This hits close to home, as a number of years ago my mother spent ten days in intensive care recovering from severe sepsis, believed to be caused by a splinter from the garden.


3. Legionellosis

Standing pools of water may hold Legionella pneumophila, the bacteria causing Legionnaires’ disease, more commonly known to be associated with outbreaks from contaminated air conditioning systems in buildings.
Related bacteria, Legionella longbeachae, are found in soil and compost. In 2016 there were 29 confirmed cases of legionellosis in New Zealand, including a Wellington man who picked up the bug from handling potting mix.
Another ten cases were reported in Wellington in 2017, again associated with potting soil. In New Zealand and Australia, Legionella longbeachae from potting mix accounts for approximately half of reported cases of Legionnaires’ disease. There were around 400 total cases of Legionellosis in Australia in 2014.
The bacteria is usually inhaled, so wearing a dust mask when handling potting soil and dampening the soil to prevent dust are recommended.


4. Melioidosis

An additional concern for residents of northern Australia is an infection called melioidosis. These bacteria (Burkholderia pseudomallei) live in the soil but end up on the surface and in puddles after rain, entering the body through cuts or grazes, and sometimes through inhalation or drinking groundwater.
Infection causes a range of symptoms, such as cough and difficulty breathing, fever or sporadic fever, confusion, headache, and weight loss, with up to 21 days before these develop.
In 2012, there were over 50 cases in the Northern Territory leading to three deaths, with another case receiving publicity in 2015. Preventative measures include wearing waterproof boots when walking in mud or puddles, gloves when handling muddy items, and, if you have a weakened immune system, avoiding being outdoors during heavy rain.


5. Rose gardener’s disease

A relatively rare infection is sporotrichosis, “rose gardener’s disease”, caused by a fungus (Sporothrix) that lives in soil and plant matter such as rose bushes and hay. Again, infections through skin cuts are most common, but inhalation can also occur.Skin infection leads to a small bump up to 12 weeks later, which grows bigger and may develop into an open sore. An outbreak of ten cases was reported in the Northern Territory in 2014.
Aspergillus, usually Aspergillus fumigatus, and Cryptococcus neoformans are other fungi that can cause lung infections when inhaled, usually in people with weakened immune systems. Gardening activities such as turning over moist compost can release spores into the air.
Of course, there are plenty of other dangers in the garden that shouldn’t be ignored, ranging from poisonous spiders, snakes and stinging insects, to hazardous pesticides and fungicides, poisonous plants, and physical injuries from strains, over-exertion, sunburn, allergies, or sharp gardening tools.


So enjoy your time in the garden, but wear gloves and shoes, and a dust mask if handling potting soil or compost. And be aware if you do get a cut or scrape then end up with signs of infection, don’t delay seeing your doctor, and make sure you let them know what you’ve been doing.


This article was originally Here  

Mary Shelley’s 200-year-old tale is still essential reading for scientists

Kai Kupferschmidt

In January 1818, a woman barely out of her teens unleashed a terrifying tale on the world: the story of a doctor who builds a creature from scavenged body parts, then recoils in horror, spurns it, and sees his friends and family destroyed by the monster. Two hundred years later, Mary Shelley’s Frankenstein is still essential reading for anyone working in science. The ill-fated creator she portrays has influenced public perception of the scientific enterprise unlike any other character, forever haunting the borderland between what science can do and what it should do.

The story has mutated and it has frequently been mangled. It has spawned countless books, plays, and movies—some pictured on these pages—and even a super- hero comic. It has inspired technophobes and scientists alike. “Franken-” has become a passe-partout prefix for anything deemed unnatural or monstrous.

Interpretations of the tale have also multiplied. A story of scientific hubris, a creator consumed by his creation, a male scientist trying to eliminate women’s role in reproduction, an attempt by Shelley to deal with the trauma of losing a baby. To the growing group of scientists pondering the ways in which science might eventually destroy humanity, it is the earliest warning of such risks.

None of this quite captures the secret of the story’s longevity. To borrow the monster’s own description of indelible knowledge, Shelley’s tale “clings to the mind … like a lichen on the rock.” In the preface to the 1831 edition, Shelley wrote: “Now, once again, I bid my hideous progeny go forth and prosper.” It did. And it still does. 

あなたの「グルテン感受性」は小麦に含まれる別の成分で説明できるかもしれない

Clarissien RAMONGOLALAINA

もしあなたがセリアック病(いわゆるグルテン過敏症)だと診断されていないけど、グルテンのせいでお腹の調子が悪いと思っているのなら、科学者たちはついにあなたの身体で何が起こっているかについての手がかりをつかんだかもしれない。「グルテン感受性」は存在しないのではないかという研究結果が出てきたのだ。たくさんの人がパンを食べた際に胃腸の不調を訴えるようだが、ある研究がその症状はおそらくグルテンと無関係であり、原因は小麦に含まれる他の成分だと示した。

セリアック病は小麦、ライ麦、大麦、オーツ麦などの穀物に含まれるタンパク質であるグルテンに対する免疫応答として知られている。様々な研究によると、一般的に約1.3%の人がセリアック病である。しかし、小麦を食べた際に不調を訴える人の割合は1.3%よりはるかに高い。セリアック病ではないがグルテン感受性を持つ人(NCGS; non-coeliac gluten sensitivity)の正確な割合は知られていないが、13%ほどもいる可能性があると示した研究結果がある。グルテンが犯人でなさそうだとわかったため、本当は何が原因なのかを調べる研究が増えてきた。

オーストラリアのモナシュ大学のピーター・ギブソンの研究チームはNCGSについて研究をすすめ、原因が短鎖炭水化物にあるかもしれないと発見した。短鎖炭水化物はFermentable Oligosaccharides, Disaccharides, Monosaccharides, Polyolsの頭文字をとってFODMAPとしても知られている。この短鎖炭水化物は腸で発酵しやすく、そのせいでお腹の張りや他の症状が引き起こされる。2014年のある研究では、FODMAPが少ない食事をするとこうした不快な症状が軽減されることが示された。

そして、ギブソンの研究チームは胃腸の症状とFODMAPの一種であるフルクタンの間に相関関係があることを見出した。彼らはセリアック病だと診断されたことがなく、グルテンフリーの食事(グルテンを全く含まない食事)をしている人を59人集めた。その被験者たちには特別に配合したミューズリーのバーを7日間食べてもらった。被験者を3つのグループに分け、あるグループにはグルテンを含むバー、別のグループにはフルクタンを含むバー、また別のグループにはグルテンもフルクタンも含まないバーを食べてもらった。

被験者はささいな症状でもアンケートに記入する決まりで、最初の7日間バーを食べたあと一週間食べるのを止め、それから別のタイプのバーを食べてもらった。この研究は二重盲検、つまり被験者も研究者も被験者が食べているバーがどれなのかを知らなかった。

最終的に、59人の被験者は皆3種類のバーをすべて食べ、研究者は被験者が食べた成分と症状を比較した。研究チームは、グルテンもフルクタンも含まないバーに比べ、フルクタンのバーは15%も多くお腹の張りを引き起こし13%も多く胃腸の症状を引き起こした。一方で、グルテンもフルクタンも含まないバーとグルテンのバーではこれらの症状に差はなかった。

この結果はNCGSの症状を和らげるためにグルテンフリーの食事をする人が全快しない理由を示している。フルクタンは小麦、ライ麦、大麦などの穀物に含まれるが、アーティチョーク、アスパラガス、にんにく、玉ねぎなどの他の食べ物にも含まれる。 

ギブソンはNew Scientistに「今まではセリアック病と、小麦を含む食事をやめたら症状が和らぐという事実からグルテンが犯人だと思われていたが、ついにその予想は間違いだと考えられる」と語った。

 

この研究はGastroenterologyに掲載された。

How do type 2 diabetes mellitus (T2DM) develop?

by Dr Malcolm Kendrick

Diabetes develops relatively slowly. You do not wake up one morning to find that you have got diabetes. For example, it has been known for many years now that women who are pregnant can develop ‘gestational diabetes.’ That is, a high blood sugar level that reveals itself during pregnancy, then goes away again after the birth.

Gestational diabetes normally returns in any subsequent pregnancy, and goes away again. Then, some years later, the woman will probably be diagnosed with diabetes. It appears from this, that pregnancy reveals an underlying progressive problem.

This slow(ish) progression is true of almost everyone else, and it usually goes through different stages. The first stage, before there are any symptoms, or any other signs, is an increased insulin response to a glucose test. A glucose test is where you feed someone a defined amount of glucose, usually seventy-five grams. This causes the blood glucose to rise quite rapidly. The sugar level peaks, then falls back to normal within about two hours. That would be considered normal.

If the insulin level rises higher after a standard oral glucose tolerance test (OGTT) this is usually the first sign that diabetes may be on the way. This can probably best be considered to represent the body trying, and succeeding, in overcoming resistance to the effects of insulin**. During this stage the blood sugar levels are normal completely.

·      Stage two: The insulin level rises higher, and the blood sugar level rises moderately higher as well. This is often called an impaired OGTT, or simply IGT (impaired glucose tolerance). The blood sugar will fall back to ‘normal’ though it may take longer to do so than in a perfectly healthy person. The fasting blood sugar will also be normal.

·      Stage three: The fasting sugar level is higher than normal. Defined as an impaired fasting glucose level (IFG). The level will not be high enough to be called diabetes. In those with IFG insulin and sugar levels both rise much higher after an OGTT, and take longer to come back down again.

·      Stage four: The fasting blood sugar level is high enough to be called diabetes. The OGTT causes a much higher ‘spike’ in the blood sugar level, and type II diabetes is diagnosed. (At this point the insulin response to the OGTT may become ‘burnt out’, so the release of insulin will often be lower than expected).

The length of time it takes to travel from ‘normal’ through stage one to stage four can be decades. It can be much less. We are now seeing more and more children with stage four (frank diabetes), so it can obviously develop quite rapidly.

Of course, these stages are somewhat arbitrary, and the definitions of impaired glucose tolerance moving to impaired fasting glucose are not fixed. The decision as to when you diagnose diabetes also depends on specific glucose levels – which have little basis in any solid data. In fact, as I write, I can guarantee that people will be deciding that the levels of blood sugar used to define diabetes are too high, and should be lowered. The sounds of money tinkles gently in background.

There has already been the relatively recent movement to create the condition known as pre-diabetes. This means that you are not diabetic yet (using the current figures for diagnosis), but you soon will be. This process is primarily driven by pharmaceutical companies who are desperate to ‘treat’ ever lower blood sugar levels with life-long medication.

Of course, to an extent, the pharmaceutical companies are right. Why do we only try to treat people at the point when their blood sugar reaches some arbitrary point? Surely we should be treating them earlier to stop them reaching this point in the first place. Well that makes sense…. But only if it works.

Equally, most people with some level of impaired glucose tolerance usually have other, potentially damaging things, going on. This was first really highlighted by Gerald Reaven. He recognised that a number of people who had raised blood sugar levels, but who were not yet diagnosed with diabetes, had a consistent spectrum of metabolic and physiological abnormalities. Sometimes called the metabolic syndrome: To quote Wikipedia:

‘The main sign of metabolic syndrome is central obesity (also known as visceral, male-pattern or apple-shaped adiposity), overweight with adipose tissue accumulation particularly around the waist and trunk.

Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level (VLDL triglyceride), impaired fasting glucose, insulin resistance, or prediabetes.

Associated conditions include hyperuricemia, fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease, polycystic ovarian syndrome (in women), erectile dysfunction (in men), and acanthosis nigricans (dark lines on the skin).’

In fact, there are a whole series of other abnormalities as well. Such as increased blood clotting factors, high levels of inflammatory markers, high levels of ceremides and diglycerols… the list is long.

Just to confuse the picture a little more, metabolic syndrome has gone by a number of other different names:

·      Reaven’s syndrome

·      Syndrome X

·      Pre-diabetes

·      Insulin resistance syndrome

Whatever it was, or is, called, it is clear that there are stages before frank Type 2 diabetes is diagnosed, where serious damage is already being done. Various researchers have found that those with the metabolic syndrome have nearly the same risk of CVD as people with diabetes.

Here is a short quote from a paper called ‘Metabolic syndrome and risk of cardiovascular disease: a meta-analysis.’

‘This analysis strongly suggests that the metabolic syndrome is an important risk factor for cardiovascular disease incidence and mortality, as well as all-cause mortality. The detection, prevention, and treatment of the underlying risk factors of the metabolic syndrome should become an important approach for the reduction of the cardiovascular disease burden in the general population.’1

Perhaps we should rename diabetes completely. Instead of IGT (impaired glucose tolerance) IFG (impaired fasting glucose) and then diabetes. We should call this metabolic condition stage 1, 2 or 3 diabetes. Maybe I should not suggest this, as the pharmaceutical companies will soon be out with even more medications, to be used even earlier. Then we will all be bankrupt.

In fact, at one time there was an attempt to define metabolic syndrome as a disease. I am not quite sure how one creates a disease from a syndrome. I think you just keep saying it often enough until it happens. I presume that the plan was to find a treatment for metabolic syndrome. To quote:

Most people may not have heard of metabolic syndrome, but that is likely to change. Once known mysteriously as syndrome X, the condition, a precursor to heart disease and type 2 diabetes, is about to be transformed into a household name by the US pharmaceutical industry and its partners in the medical profession. A society dedicated to addressing the condition has been organised, a journal has been started, and an education campaign launched. Patients are already being tested for metabolic syndrome. As the trade publication Pharmaceutical Executive said in its January 2004 issue: ‘A new disease is being born.’2

Since then… nothing much has been heard of this initiative. Why not? Well, if the metabolic syndrome is the underlying problem in a whole series of other conditions, and it probably is, then if the metabolic syndrome went away, all of the associated conditions would simply go away too. No more high blood pressure, low HDL and high VLDL (dyslipidaemia), obesity, impaired blood glucose levels fatty liver, erectile dysfunction etc. etc.

Thus, if you actually managed to cure metabolic syndrome, about half the medications prescribed around the globe would no longer be needed. Tens of millions of people would no longer need high blood pressure medication. The market for T2DM would shrivel up and die. Pharmaceutical company profits would be annihilated overnight. So, we hear little about metabolic syndrome anymore.

However, despite the rapid rise and subsequent disappearance of the metabolic syndrome, it does raise a critical issue. Namely that diabetes is far from a simple condition where the blood sugar level is high – end of. A whole range of other potentially damaging factors are deranged at the same time. Any, or all of which could cause the health problems associated with diabetes. Perhaps the blood sugar level doesn’t really matter at all. It is just a marker for underlying metabolic dysfunction.

I am not saying that this is necessarily the case, but the possibility does not even seem to be considered. At present the very strong impression given, and unconsciously accepted, is that diabetes is almost entirely about blood sugar levels, and insulin. If the sugar is high, this is bad. If it is low, this is good. On the other hand, insulin is good, because it lowers blood sugar levels.

This simple meme was evolved to a large extent after the discovery of the role of insulin in Type 1 diabetes. Children who have diabetes have a lack of insulin. If you give them insulin, their sugar levels fall, and they become well again. Thus it has been accepted that sugar is bad, insulin is good. However, it was never the high sugar levels that killed them. It was the keto-acidosis caused by fatty acids escaping from adipose tissue. A completely different metabolic problem. And, of course, if your blood sugar level falls too low, this will kill you quicker than anything else. Sugar bad?

Dr Malcolm Kendrick

@malcolmken

drmalcolmkendrick.org

The Great Cholesterol Con, John Blake Publishing Ltd, 2007

Doctoring Data: How to sort out medical advice from medical nonsense, Columbus Publishing Ltd, 2014

Tiniest and cutest Lemur From Madagascar

The African island of Madagascar is a magical hotspot of biodiversity found nowhere else on the planet – and that includes being the native home of every lemur in the world. The cuddly primates comprise a total of around 100 species, with new ones being categorised ever so often. Now researchers have described the latest addition to the dwarf lemur family, the Groves’ dwarf lemur Cheirogaleus grovesi.

The nocturnal critter, measuring just 17 centimetres (6.7 inches) with a lush 28-centimetre tail, is a brownish-black lemur with a cute white patch on the nose. Like all its cousins, it also sports massive, heartbreakingly cute dark eyes, and tiny little fingers with opposable thumbs that help with tree climbing and fruit picking.

Groves’ dwarf lemur lives in the southeastern parts of the island, and was found in two national parks – Ranomafana and Andringitra, where it lives in the rainforest canopy and subsists largely on fruit. The species has been named in honour of renowned British-Australian primatologist Colin Groves “in recognition of his more than 40 years of work in the fields of primatology, evolutionary biology, morphological analysis, mammalian taxonomy and associated disciplines.”

Groves, who passed away last year, identified more than 50 animal species during his long career. That included several new dwarf lemurs back in 1999, when it was still thought the family contained only two species – a number that’s now swelled to eight in total.

While lemurs within a genus such as Cheirogaleus can look strikingly similar to each other, advances in molecular DNA analysis have allowed for more fine-grained identification of distinct species, as in the case of this latest find.

The team collected small DNA samples from several lemurs safely caught and subsequently released back into the rainforest, and compared the mitochondrial sequence data to samples from previously described and proposed species in 2014 and 2015. And the researchers believe we can expect to meet even more lemur species in the coming years.

“This new species is one of several new dwarf lemurs in the genus Cheirogaleus that have been or are in the process of being described,” one of the research team, Russell Mittermeier from Global Wildlife Conservation told Mike Gaworecki at Mongabay.

“It is indicative of how little we know about biodiversity in general, and even of our closest living relatives, the primates.”

Many lemur species are threatened or endangered – the team notes that Groves’ dwarf lemur’s conservation status is currently unknown, but it could be fairly well sheltered because it lives in a protected area.

Still, they note that more work will be needed to give it a proper categorisation, and to help shield this darling little animal and its brethren from potential extinction.

“The continuing identification of new primate species in Madagascar’s remaining wild places highlights the need to protect this habitat from additional disturbance by human encroachment,” the team writes in their paper.

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愛ある食糧生産:ロラニエ神父によるマダガスカルの稲作

Clarissien RAMONGOLALAINA

私の国、マダガスカルはアフリカ南東部に位置し、植物や動物の固有種を持つ島として有名です。マダガスカルは、名食文化で米の摂取種は年間一人当たり120kgと言われています(日本の2倍)。昔ながらの農法とインフラ整備の結果、現在では米の一部は輸入していますが、その数値は20%ほどです。(http://www.irinnews.org)。気候変動に直面すると、全米の米需要を満たすことはさらに困難になります。さらに、マダガスカル農家は、土地の縮小、資本へのアクセス、教育、肥料としてのインプットへのアクセス、土壌の肥沃度、情報の不均等な分配、水と土地の劣化などの社会経済的および環境的問題に直面しています。


マダガスカル政府は、国の食糧生産の自給率を高め、国民の人口増加に追いつくために、SRI 農法(System of Rice Intensification, 稲集的栽培法)と呼ばれる米の生産性を高めるための新しい技術を推進しています。SRIは、フランスの宣教師であるロラニエ神父 (Henri de Laulanie: 1920 – 1995)によって1980年代初めにマダガスカルで開発されました。1990年代半ば以降、SRIは小さいなNGOであるTefy Saina (http://ciifad.cornell.edu/)によって注目され普及されてきました。SRIは最先端の難しい技術を駆使した近代的農業技術ではなく、苗の大きさや肥料や水管理といった誰にでもできる手法を組み合わせたものですが、その方法はこれまでの稲作の常識を覆すものです。SRIは収量の増大のみならず、環境を破壊しない持続的な農法として認められています。ただ、マダガスカルの多くの農家は先祖伝来の方法を変えようとせず、SRIを認めない農家多いのが現状です。SRIはまさに技術先行であり、収量増加について科学的な説明が追いかけていると言えます。現在は、SRIが非常に理にかなった手法であるとが明らかになっており、すでに世界の55カ国以上で採用され、数百万の規模米稲作農家の稲生産に貢献しています。


ロラニエ師が1961年にマダガスカルに神父として来た時、この国の貧困に驚き、この国に大事なのは7人の神父よりも一人の農学者である、と言ったそうです。ロラニエ神父はマダガスカルで自分がすべきことを考えた結果、稲を通じて多くの人を助けた神父様です。ロラニエ神父の人を助けようする心、必死に稲を観察し、自分にできることに専念したことに感動いたします。ロラニエ神父は1995年にマダガスカルでなくなり、マダガスカルの地に眠っておられます。私は、今日本で稲作や稲の品種改良の研究をしています。私も稲を通じて多くの人たちと関わりを持ち、一人でも多くの人々に貢献できるよう頑張っています。

小麦が塩分の多い土地で生き抜く可能性

Clarissien RAMONGOLALAINA

マングローブほど塩が好きだというわけではないだろうが、小麦がその海浜植物と共通の性質を持っていることを科学者たちは発見した。オーストラリアの分子育種の共同研究センターのYusuf
Genc
博士はさまざまな小麦がさまざまな方法で塩分に対応していることを発見した。塩分に耐性のある植物を栽培する方法を長い間探している穀物農家にとってこの研究は意味がある。塩分と言われて、ほとんどの人はどんなに強い作物でも育たない、広大な不毛の土地を想像するだろう。しかし、こうした乾燥した土地はオーストラリアの塩分の問題のほんの一部である。土壌に含まれる塩分の季節性変動はオーストラリアの農業経済において毎年13億ドルもの損失の原因である。

 

オーストラリアの乾燥農地の約67%が塩分の季節性変動を起こす可能性があり、起こってしまうと作物の生産量が減る。研究者たちはこれまで塩分に耐性のある新しい作物を生み出そうとしてきたが、その成功は本当に限られたものだった。しかし、小麦が塩分に対処するメカニズムを利用すれば、農家は塩分に耐性のある作物を選べるだろう。「50年も塩分耐性について研究を続けてきたのに、塩分耐性を持つ作物はほとんど生みだされなかった」とGenc博士は語る。

 

Genc博士によると、塩分を排出することだけがメカニズムではないようだ。むしろ、マングローブに似て、ある種の小麦は塩分を根から吸い上げるがその塩分にあまり影響を受けない。「この分野の研究をしているたくさんの人が植物が塩分を排出する能力を上げようとしている。私たちの研究によって塩分の排出だけがメカニズムではなく、むしろある種の小麦は塩分を吸い上げそれに耐性を持つと示された。」とGenc博士は語る。

 

「組織耐性」として知られるこのメカニズムは、他の種の小麦に適用されれば、塩分に悩まされている農家にとって生産量の劇的な増加につながるかもしれない。Genc博士の研究チームはBerkutKrichauffという二つの小麦を様々な塩分濃度において栽培し、吸い上げた塩分の量と収穫量を評価した。

 

どちらも塩分耐性が高い植物として知られているが、彼らはBerkutKrichauffほど塩分が入ってくるのを防げないことを発見した。そのかわり、BerkutKrichauffと同じくらい収穫量があった。「この現象ははじめ理解に苦しむものでした。なぜなら従来、研究者たちは塩分濃度が高ければ塩分耐性が低いと考えていたからです。しかし、私たちはこれらの2つの小麦では2つのメカニズムが働いていると気付きました。」とGenc博士は語る。

 

塩分の排出能力を持つ種もあれば、組織耐性を持つ種もある。「もしそのような種を同時に栽培すると、植物に含まれる塩分量と塩分耐性の関係はなくなるでしょう。私たちの研究は塩分の排出がすべての種で働いている唯一のメカニズムではないことを示しました。」Genc博士は語る。塩分耐性の生理学をより深く理解することによって、彼らは塩分耐性を持っているかどうかのスクリーニングをするための、遺伝的な「指紋」のようなDNAマーカーを同定しようとしている。今年の後半に予定している実験によって彼らは農地でも同じ効果が得られることを期待している。

 

「私たちは2ヶ所の土地を選んだ。どちらの土地も塩分に影響される土地である。実験をするのが待ちきれない。この実験から得られる結果は塩分耐性小麦の開発に向けての大きな一歩になるだろう。」とGenc博士は語る。

この研究はここに掲載された。


What is ice cream in science? How to make a perfect ice cream?

by Clarissien Ramongolalaina

While the true origins of ice cream are somewhat unclear, there are a number of stories describing how ice cream was first created in ancient China via Marco Polo and other tales of the Roman Emperor Nero sending slaves to the mountains to collect snow for an ice creamlike treat. The rise in popularity and availability of ice cream certainly correlates to key scientific advances, particularly the concept of freezing point depression. The principle of freezing point depression states that adding a salt (solute) to an ice water mixture (solvent) reduces the temperature at which the mixture freezes.

Ice cream is far from being a solid frozen bowl of cream. In fact, ice cream is a mixture of solids (ice and partially frozen milk fat), liquid (unfrozen cream and sugar water), and pockets of air trapped in the freezing mixture by mixing. These three phases are scattered among each other forming a colloid. A colloid is a mixture with properties of homogeneous and heterogeneous mixtures and is formally defined as a microscopically dispersed mixture in which dispersed particles do not settle out. Ice cream can be described as an emulsion and a foam, both of which are examples of colloids. The formation of an emulsion (the solid phase of frozen fat globules and ice water distributed through the liquid phase of sugar water and cream) is typically unstable, but proteins and lipids coat the fats and stabilize the mixture from collapsing into two separate fat and water phases. These mediators between fat and water phases are called emulsifiers. The foam nature of ice cream is due to the trapped pockets of air created as the freezing cream is mixed. Overrun is the increase in volume of the ice cream before and after mixing due to this trapped air. Some ice cream can have an overrun of nearly twice the volume of the ingredients before freezing and mixing.

The ratio of each phase of the colloid is critical for the mouthfeel and creaminess of the ice cream. Too much fat and the ice cream will have the consistency of butter, too much sugar or milk solids creates a weak ice cream, while the emulsifiers limit the amount of crystals keeping the ice cream from becoming crunchy.

Federal standards (21 CFR § 135.110) require that ice cream contain a minimum of 10% milk fat and 20% milk solids—the solids refer to proteins and sugars like lactose or sucrose. Most ice creams include stabilizing emulsifiers to minimize the formation of ice and fat crystals that decrease the taste of ice cream. Fat is important for taste, providing both a creamy feel to the tongue and sweetness. The proteins and sugar add body or chewiness to the ice cream. A number of different stabilizers or emulsifiers can be found in ice cream. Added whey protein or gelatin protein from muscle tissue is used to coat the fat and provide the body. Custards use egg yolks, which have the phospholipid lecithin as an emulsifier. Another commonly used emulsifier is Polysorbate 80. This is a complex carbohydrate with a long unsaturated fatty acid bonded to it. As an emulsifier in ice cream, Polysorbate 80 can be found in fairly high concentration where it keeps the ice cream scoopable. The carbohydrate portion of the molecule interacts with water and protein, while the fatty acid tail of Polysorbate 80 hydrophobically interacts with the fat globules. This coating keeps the fat and water phases together. Stabilizers include complex carbohydrates (starches and gums) and are commonly found in the ingredient list of commercial ice cream. A common additive used to reduce the formation of ice crystals is alginate. Also a complex carbohydrate, alginate is isolated from the cell walls of algae. Alginate contains many OH functional groups and readily binds water through hydrogen bonding. The extensive hydrogen bonding of alginate limits the flow of water and forms a gel that acts as thickener. The organization of the water–carbohydrate complex also defeats the formation of ice crystals. The cell wall carbohydrate from red algae (seaweed), carrageenan, is used in place of alginate in many foods.

Ice cream can come in many confusing grades and styles. Superpremium and premium ice cream has low overrun and high fat content with the best quality ingredients. Standard ice cream has more overrun (air) than superpremium or premium ice cream and meets the minimum requirements of 21 CFR § 135.110. Fatfree ice cream has less fat than the CFR standard and must have less than 0.5% fat per serving. In contrast, light ice cream is a description of the amount of calories coming from fat. Light ice creams must have less than half of its total calories per serving from fat. Low and reduced fat ice creams fall somewhere between light and fatfree in their fat composition. Standard vanilla ice creams, also called Philadelphiastyle ice cream, differ from French vanilla in that Frenchstyle ice creams, like custards, use egg yolks as an emulsifier, while standard or Philadelphiastyle ice creams (also called New York) use no egg or just the egg whites. Gelato is a frozen ice creamlike dessert that has higher fat and almost no overrun. Sherbet stretches the ice creamlike properties with fruit juice and some milk fat, whereas sorbet is not an ice cream at all! Sorbet contains no milk or cream and is instead a frozen puree of fruit with added alcohol or wine to reduce freezing temperature. Soft serve ice cream is low fat (3–6%) with up to 60% air overrun.

Making ice cream is pretty straightforward and while an ice cream maker helps, it can be done without a machine. A simple base recipe is a combination of milk, heavy cream, sugar, and salt. From this base, flavorings including vanilla and chocolate can be added and are as diverse as there are ice cream creations. Richer custard or Frenchstyle ice creams include adding egg yolks as emulsifiers followed by heating and cooling the mixture. Cream and milk are added to a mixture of egg yolk and sugar, which is then cooled before freezing. With your ice cream mixture complete, you are ready to freeze it, but now comes the work! Air must be introduced, crystallization must be limited, and the fat and liquid phases must be kept together while freezing. This is all accomplished by mixing. Mixing can be accomplished by hand by placing the liquid ice cream into a larger container of ice, water, and salt. The salted ice bath will have a lower temperature than ice water alone allowing the sugar and fat water “ice cream” to freeze. Ice cream makers maintain a constant mixing as the liquid ice cream mixture begins to freeze. Once frozen, the ice cream can be eaten or left in the freezer to “harden.” At freezer temperature (−4°F/−20°C) about only 75% of the water is frozen, and the rest is a liquid sugar–water mixture. Rapid and deep freezing causes most of the liquid water to freeze without forming unwanted crystals. Partial thaw and refreeze cycles will increase the amount of the liquid phase, and larger crystals will form, giving the ice cream an offtaste and crunchy tooth feel (texture).    

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