HIGH SCHOOL SHOULD START AT 10 TO 11

A study by researchers from the University of Oxford, Harvard Medical School and the University of Nevada has found that current school and university start times are damaging the learning and health of students

Drawing on the latest sleep research, the authors conclude students start times should be 08:30 or later at age 10; 10:00 or later at 16; and 11:00 or later at 18. Implementing these start times should protect students from short sleep duration and chronic sleep deprivation, which are linked to poor learning and health problems.

These findings arise from a deeper understanding of circadian rhythms, better known as the body clock, and the genes associated with regulating this daily cycle every 24 hours.

It is during adolescence when the disparity between inherent circadian rhythms and the typical working day come about. Circadian rhythms determine our optimum hours of work and concentration, and in adolescence these shift almost 3 hours later. These genetic changes in sleeping patterns were used to determine start times that are designed to optimize learning and health.

The US Department of Health has also recently published an article in favor of changing the start times for Middle and High Schools.

Corresponding author Paul Kelley (Honorary Clinical Research Associate, Sleep and Circadian Neuroscience Institute, University of Oxford) will be presenting Time: the key to really understanding our lives at the British Science Festival on Tuesday 8 September.

Neuropathy Remedies Should Cost Less

Today's post from sciencedaily.com (see link below) talks about the scandalous difference in the costs of drugs used to treat the symptoms of neuropathy. As so often, the emphasis is on diabetic neuropathy but as most readers will know by now, neuropathy is neuropathy, irrespective of the cause. Once the cause has been established, the treatment is pretty much the same for all painful neuropathies. Drug companies do have to promote their drugs and there are costs involved with getting official approval but the fact is that the profit margins are enormously high in a 'captive' market where treatment paths have remained pretty much the same for decades. This can lead to people missing out on vital symptom-reducing treatments, especially in other parts of the world, where insurance systems are less inclusive. Prices do drop when patents run out and generic versions take their place but in the meantime, drug companies make hay while the sun shines!

Cost and effect: Cheaper remedies should rule for diabetes nerve pain  University of Michigan Health System November 5, 2014

Millions of people with diabetes take medicine to ease shooting, burning nerve pain, and new research suggests that many medicines can offer relief. But since some of those medicines cost nearly 10 times as much as others, cost should be a crucial factor in deciding which medicine to choose for diabetic neuropathy, say experts.

Millions of people with diabetes take medicine to ease the shooting, burning nerve pain that their disease can cause. And new research suggests that no matter which medicine their doctor prescribes, they'll get relief.

But some of those medicines cost nearly 10 times as much as others, apparently with no major differences in how well they ease pain, say a pair of University of Michigan Medical School experts in a new commentary in the Annals of Internal Medicine.

That makes cost -- not effect -- a crucial factor in deciding which medicine to choose for diabetic neuropathy, or diabetes nerve pain, the U-M researchers say.

Their commentary accompanies a paper from Mayo Clinic researchers and their colleagues, who analyzed a wide range of data from clinical trials of different treatments for painful diabetic neuropathy. The Mayo-led team concluded that several options appear to work well, though they need to be compared head-to-head to tell for sure which is best.

Until new studies can make those head-to-head comparisons, say the U-M experts, doctors should consider the cost of the drug, and any other conditions a patient has, when deciding what to prescribe.

Brian Callaghan, M.D., the article's first author, says the new Mayo study, national guidelines and other efforts have focused on how well different treatments work against diabetic nerve pain. Half of all people with diabetes develop neuropathy sometime during their experience with the disease, and it can keep patients from exercising or walking. Neuropathy plays a role in many diabetes complications.

But cost hasn't figured into these studies, he says. That's why he and fellow U-M neurologist Eva Feldman, M.D., Ph.D., decided to look at the dollars side of diabetic neuropathy for their article.

"These treatments all work about the same, but what's different is their side effects and cost. The older medications are an order of magnitude cheaper, about $15 to $20 a month, compared with the newer ones at nearly $200 per month," he says. "Patients are on these medications for many years, and it really starts to add up. Given that the effects of the medications are similar, why should we start patients on the expensive drugs until we've determined whether or not they respond to the less-expensive ones?"

The newer drugs, of course, have marketing campaigns behind them -- and in the case of diabetic neuropathy, their manufacturers may have sought and received specific approval for diabetic neuropathy from the Food and Drug Administration.

The newer drugs have earned the highest level of recommendation in national treatment guidelines, which requires that at least 80 percent of people taking part in a clinical trial complete it in order for the study to be considered for high-level guideline approval. This helps create an artificial appearance that the newer drug is the better choice, says Callaghan.

But in fact, the trials of other medications for diabetic neuropathy had 70 percent or more completion rates, he says -- not an appreciable difference.

And even though older generic drugs without a specific indication for diabetes pain must be prescribed "off label" by doctors, the evidence that they work is powerful -- including the evidence from the new meta-analysis by the Mayo-led team.

Callaghan, who sees diabetic neuropathy patients at the U-M Health System, says he prescribes generic drugs, gabapentin or one of the tricyclic antidepressants, routinely as the first option for new pain.

The authors looked at the cost of one month of the typical starting dose for each of these medications. According to Drugstore.com, pregabalin is the most expensive at $189.98 per month, followed by duloxetine at $170.99 per month. Although venlafaxine is generic, its cost remains high at $119.98 per month. In contrast, gabapentin comes in at $18.99 per month, amitriptyline at $12.99 per month, and nortriptyline at $19.99 per month. A topical cream of capsaicin, available over the counter without a prescription, costs the least: $13.99 per month.

"The Mayo study supports other systematic reviews on this issue," he says. "We hope that adding in the cost consideration will be useful to neurologists and primary care physicians alike, since we all treat patients with painful diabetic neuropathy."

Callaghan, an assistant professor in the Department of Neurology, is also a member of the U-M Institute for Healthcare Policy and Innovation. Feldman is the Russell DeJong Professor of neurology and director of the A. Alfred Taubman Medical Research Institute.

Story Source:

The above story is based on materials provided by University of Michigan Health System. Note: Materials may be edited for content and length.

Journal References:
Marcio L. Griebeler, Oscar L. Morey-Vargas, Juan P. Brito, Apostolos Tsapas, Zhen Wang, Barbara G. Carranza Leon, Olivia J. Phung, Victor M. Montori, M. Hassan Murad. Pharmacologic Interventions for Painful Diabetic Neuropathy. Annals of Internal Medicine, 2014; 161 (9): 639 DOI: 10.7326/M14-0511
Brian C. Callaghan, Eva L. Feldman. Painful Diabetic Neuropathy: Many Similarly Effective Therapies With Widely Dissimilar Costs. Annals of Internal Medicine, 2014; 161 (9): 674 DOI: 10.7326/M14-2157

http://www.sciencedaily.com/releases/2014/11/141105093332.htm

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MAKING SURE ANTIBIOTICS AS THEY SHOULD

Researchers at ETH Zurich are decoding the structure of the large ribosomal subunit of the mitochondria at an atomic level, thereby providing insight into the molecular architecture of this ribosome with implications for a better understanding of the mode of action of antibiotics.

A team of ETH Zurich researchers led by professors Nenad Ban and Ruedi Aebersold have studied the highly complex molecular structure of mitoribosomes, which are the ribosomes of mitochondria. Ribosomes are found in the cells of all living organisms. However, higher organisms (eukaryotes), which include fungi, plants, animals and humans, contain much more complex ribosomes than bacteria. In eukaryotes, ribosomes can also be divided into two types: those in the cytosol -- which comprises the majority of the cell -- and those found in the mitochondria or "power plants" of cells. Mitochondria are only found in eukaryotes.

Ribosomes serve as translation devices for the genetic code and produce proteins based on the information stored in DNA. Every ribosome consists of two subunits. The smaller subunit uses transfer ribonucleic acids (transfer RNA or tRNA) to decode the genetic code it receives in the form of messenger RNA, while the larger subunit joins the amino acids delivered by the transfer RNA together like a string of pearls.

Even higher resolution, even more details

Mitochondrial ribosomes are especially difficult to study because they are found only in small amounts and are difficult to isolate. At the beginning of the year, ETH researchers had shed light on the molecular structure of the large subunit of the mitoribosome in mammalian cells to a resolution of 4.9 Å (less than 0.5 nm). However, this resolution was not adequate to reliably build a complete atomic model of this previously unknown structure. The team lead by ETH Professor Nenad Ban has now succeeded in this task and was able to map the entire structure at a resolution of 3.4 Å (0.34 nm). The researchers recently published their findings in the scientific journal Nature.

The scientists used high-resolution cryo-electron microscopy at the Electron Microscopy Center of ETH Zurich (ScopeM) and state-of-the-art mass spectrometry methods in their experiments. Thanks to recent technical advances in cryo-electron microscopy and the development of direct electron detection cameras that can correct for specimen motion during the exposure, it only recently became possible to capture images of biomolecules at a resolution of less than four angstroms.

Improving the effect of antibiotics

In particular, the new images show the details of the peptidyl transferase centre (PTC), which is where the amino acid building blocks are combined. The proteins synthesised in this way then pass through a tunnel, where they finally exit the large subunit of the ribosome.

"This process is medically relevant," said Basil Greber, lead author of the study and postdoctoral researcher in Nenad Ban's group. The reason is that this tunnel is a target for certain antibiotics. The antibiotic becomes lodged in the tunnel and prevents the proteins that have just been synthesized from leaving the tunnel. However, antibiotics should only inhibit protein synthesis in the ribosomes of bacteria.

"For an antibiotic to be used in humans, it must not attack human ribosomes," explains Greber. Antibiotics must inhibit protein synthesis only in bacterial ribosomes. The problem is that mitochondrial ribosomes resemble those of bacteria, which is why certain antibiotics also interfere with mitoribosomes. "This can lead to serious side effects." The ETH researchers' findings will make it possible in the future to design antibiotics that inhibit only bacterial and not mitochondrial ribosomes. This is one basic requirement for using them in clinical applications.

A surprising discovery

The ETH researchers also made an unexpected discovery. They found that mitoribosomes use transfer RNA in two fundamentally different ways. Firstly, the tRNA is used to select the right amino acid for peptide synthesis in the PTC. Secondly, one tRNA is a fixed part of the structure, unlike in all other ribosomes. Although it has been known for quite some time that mitochondrial ribosomes integrated new proteins into their structure over the course of their development, this is the first time that the use of an entirely new RNA molecule was observed. "This demonstrates the great evolutionary plasticity of mitoribosomes," underscored Greber.

The ETH team is now faced with a major, still unresolved task in its research: determining the structure of the smaller subunit of the mitochondrial ribosome. The fact that it is more flexible than the large subunit renders this undertaking an even greater challenge.