Possibility Of Cracking Herpes Now Exists

Cold sores and shingles, two forms of the very annoying – and very difficult to deal with – herpes virus may no longer be as difficult to find and flush out as it has been since it was discovered. U.S.-based researchers believe they have managed to found a way to flush out the annoying little virus using a mysterious genetic trait carried by the herpes simplex-1 virus – which causes cold sores in those who are infected by it – that allows it to linger undetected in the nerves that it infects. The herpes virus, according to the research team, manages to remain in stealth mode via the use of microRNAs, small bits of genetic material that allow for the regulation of the activities of many viruses.

According to the researchers, it is possible to force the virus to become active, and then proceed to eliminate it by using standard antiviral medications. One cited example was acyclovir. This information was stated by Jennifer Lin Umbach, from Duke University in North Carolina, who was one of those who worked on the study that obtained the data. Umbach said that the team was trying to go into animal trials to determine the veracity of their assumptions.

Based on news reports, the team from Duke is engaging in discussions for a potential collaborative effort with Regulus Therapeutics LLC, a joint venture between Alnylam Pharmaceuticals, Inc and Isis Pharmaceuticals, Inc. The group is known for specializing in microRNA studies.

The herpes viruses are known for causing many permanent infections, often heading straight to the nerve cells they damage. The ability of the virus to remain dormant in the life of any given host – animal or human – can often cause periodic outbreaks to occur when the virus begins to awaken. Herpes simplex-1 causes cold sores, herpes simplex 2 causes genital herpes, and varicella can cause chicken pox in younger patients. For older patients, varicella can appear as herpes zoster, the cause of shingles. Anti-viral medications have only been known to slow the progress of the virus down, not remove it from the body outright.

The main problem I’ve seen in texts about herpes is that it can’t be killed with any treatment available if the bug is still inactive. Without the virus being active and causing damage, it simply can’t be treated or stopped. Another interesting trait of the condition is that the same virus can end up infecting different neurons in the same body, and were also able to activate the infections at different times. These two combined traits make it difficult – if not outright impossible – to wipe out an infection in a single person, let alone a widespread and dormant one. This means that discovering the gene that controls the microRNAs that trigger the active stage of the virus can go a long way in helping medical science counter the threat of herpes.

However, for the time being, this is all strictly conjecture at this point. There’s still no direct evidence saying that it would be possible to activate those genetic markers, let alone be able to activate them reliably. Still, this is currently the best lead medical science has to finding a cure for herpes, so not everything is bad.

Resource Box : Harvey Ong is currently employed as a researcher for an online media company, currently writing about pharmaceutical products and herbal remedies. He is also an amateur paleontologist and has a collection of various animal toxins, for research reasons.

Protein-Alzheimer’s Link Being Probed

Alzheimer’s. People know it. People fear it.

Unfortunately, people can’t cure it, either.

The sad part is that nobody seems to have any idea what causes this problem. There are numerous scattered theories that suggest one thing or another, but really, the medical community knows very little about the causes of this. Which sort of makes it a disease that’s exceedingly tough to cure, doesn’t it? After all, if you don’t know what’s causing a problem, you’re sort of stuck playing damage control for the effects. You can’t really solve it without knowing what the root of it is. This is, presumably, why there are so many studies going on that are trying to find out what makes Alzheimer’s tick. Once we know what causes it, maybe we can find a way to reverse the damage? Or maybe even prevent it from happening. A bit of a dream, so for now, we stick with treatment.

Well, there might be some hope along that horizon. A research team believes that they may have found a sticky little protein that could be linked to the condition. They’ve found that they caused symptoms of memory loss similar to a number of forms of dementia in rats by injecting a protein they call beta-amyloid. According to them, this protein is also present in patients with Alzheimer’s. Apparently, it forms some sort of plague-like problem that can be found in the brains of people with the aforementioned condition. Nobody’s really been able to tell whether this was the cause or just one of the side effects, though. After all, the problem shows up in people without Alzheimer’s.

Tests have been done on this protein before, I’m told. This is because, as stated, it does tend to show up in patients with Alzheimer’s. Many believed that it might have held some sort of connection to the cause of the disease. Some believed that the discovery of the protein in people without the condition negated that hypothesis, but this latest revelation is proving promising in reviving beta-amyloid as a potential avenue of research. And in the quest to find out what triggers Alzheimer’s – and how to fix the damage so that the trigger can be undone – then any given lead is as good as anything.

It should be made known that there are basically three types of the aforementioned protein. Each of them is, clearly, of the sticky variety. Each one is generally found in patients with Alzheimer’s, and in some cases, in people who don’t have the condition and have no signs of developing any form of dementia. According to the research team, the first two types did not cause any sort of dementia in the laboratory test subjects that were injected with it. Whether or not this disproves the connection with dementia is unknown. The third type of the protein, in contrast, definitely caused some effect. Most of the test rats that were injected with it developed dementia.

The question now, however, is why did this happen? And furthermore, can it be prevented?

Resource Box : Harvey Ong is currently working as a writer-researcher for an online pharmaceutical company. He has also had experience field testing blackjack betting systems and is an amateur poker player.

Protein-Alzheimer’s Link Being Probed

Alzheimer’s. People know it. People fear it.

Unfortunately, people can’t cure it, either.

The sad part is that nobody seems to have any idea what causes this problem. There are numerous scattered theories that suggest one thing or another, but really, the medical community knows very little about the causes of this. Which sort of makes it a disease that’s exceedingly tough to cure, doesn’t it? After all, if you don’t know what’s causing a problem, you’re sort of stuck playing damage control for the effects. You can’t really solve it without knowing what the root of it is. This is, presumably, why there are so many studies going on that are trying to find out what makes Alzheimer’s tick. Once we know what causes it, maybe we can find a way to reverse the damage? Or maybe even prevent it from happening. A bit of a dream, so for now, we stick with treatment.

Well, there might be some hope along that horizon. A research team believes that they may have found a sticky little protein that could be linked to the condition. They’ve found that they caused symptoms of memory loss similar to a number of forms of dementia in rats by injecting a protein they call beta-amyloid. According to them, this protein is also present in patients with Alzheimer’s. Apparently, it forms some sort of plague-like problem that can be found in the brains of people with the aforementioned condition. Nobody’s really been able to tell whether this was the cause or just one of the side effects, though. After all, the problem shows up in people without Alzheimer’s.

Tests have been done on this protein before, I’m told. This is because, as stated, it does tend to show up in patients with Alzheimer’s. Many believed that it might have held some sort of connection to the cause of the disease. Some believed that the discovery of the protein in people without the condition negated that hypothesis, but this latest revelation is proving promising in reviving beta-amyloid as a potential avenue of research. And in the quest to find out what triggers Alzheimer’s – and how to fix the damage so that the trigger can be undone – then any given lead is as good as anything.

It should be made known that there are basically three types of the aforementioned protein. Each of them is, clearly, of the sticky variety. Each one is generally found in patients with Alzheimer’s, and in some cases, in people who don’t have the condition and have no signs of developing any form of dementia. According to the research team, the first two types did not cause any sort of dementia in the laboratory test subjects that were injected with it. Whether or not this disproves the connection with dementia is unknown. The third type of the protein, in contrast, definitely caused some effect. Most of the test rats that were injected with it developed dementia.

The question now, however, is why did this happen? And furthermore, can it be prevented?

Resource Box : Harvey Ong is currently working as a writer-researcher for an online pharmaceutical company. He has also had experience field testing blackjack betting systems and is an amateur poker player.

Differing Approaches To Achieving Wellness

Everyone wants to achieve a state of better health and wellness. There are medications, treatments, exercises, shows, and books dedicated to helping people get to this proposed state. However, there is something that is being ignored amidst all this. This is something important, I think. In fact, it is probably more important than any of the advice or techniques about achieving wellness. You see, this thing is a question that people don’t seem to be answering. If they are answering it, the answer either isn’t very clear or conflicts with what everyone else seems to think the answer is. No, I’m not talking about life itself. Everyone knows life means ’42.’ What I’m talking about is what does it actually mean to “achieve wellness?”

Most of the medical establishment tends to recapitulate the same words and phrases that comprise that is seen to be standard wisdom for achieving wellness. Watch your diet. Exercise regularly and properly. Drop the extra pounds that you have. Quit smoking. Have your body screened regularly for various dire illnesses so you can avoid problems early on. Keep your blood sugar and cholesterol levels as low as you can. Keep in touch with your primary medical provider, and have any aches and pains checked out – they might be signs of even worse problems. These things are what the medical establishment wants you to remember; these are the things they saw will help you achieve wellness and better physical health. Still, there are those who choose to dissent – and some of them are from the medical community itself.

According to a certain Dr. Hadler, all the fitness and health in the world can’t undo one simple fact: we’re all going to die. No, he doesn’t have a skull decorating his desk, but that would add a touch of visual confirmation of his view. He says that all the good stuff in the world isn’t going to do much help against the ravages of time and aging. There is no way to hold off every dire illness in existence at bay for eternity, much less something as unstoppable as time. The fact is, permanent wellness is simply impossible to achieve – it isn’t even a real option. He says that the real goal should be reaching a ripe, venerable age with most of one’s core physical abilities still largely intact – no loss of hearing, sight, bodily functions, and the like. He also says that if you want to achieve that long-term goal, ignoring the medical establishment is the easiest way to do it.

The fun part is that both these sets of advice are from people in the medical establishment. That simple little detail means that they both have a rather large degree of credibility. The question becomes which one is really the more accurate one. That isn’t so easy, because on one hand, Hadler is right in saying that you’re going to die eventually, so delaying it shouldn’t even be considered an option. On the other, nobody really wants to die and doing a lot of healthy things can not only delay death, but also decrease the risk of dying in certain ways.

Resource Box : Harvey Ong is a part-time writer and a part-time researcher. He is currently self- studying various Far Eastern languages and is an avid fiction reader. He is currently writing articles oriented towards consumers of pharmaceutical products, but has written about used car loans, gambling and casino strategies, and overseas travel in the past.

Old Drug, New (Cancerous) Horizons

Competition, they say, is one of the reasons for innovation and development. So long as one group isn’t trying to sabotage the other and is legitimately working on their project, things should go fine. This has been applied to everything from business to weapons development, and it has worked. So really, you and I should not be shocked to learn that something like this is going on in the twisted little world we know as medicinal research. The way most pharmaceutical and medical research companies go about their business is highly driven by competition – the urge to get the product out and start raking in the profits for it. Only in rare situations will the competitive nature of the game actually make two companies meet in battle at one of the biggest cancer conferences in the world and both leave standing tall.

Incidentally, this is also good news for cancer patients.

You see, data presented at the aforementioned conference is predicted to boost the sales of a drug called Erbitux. The drug, developed and sold by ImClone Systems, is expected to see increased use as an initial medication for patients that have advanced cases of lung and colorectal cancers, thanks to this data. However, others believe that this increase in revenue might come at the cost of the drug Avastin. Avastin, made by a company known as Genentech, has long been used as the frontline pharmaceutical treatment for the cancers previously mentioned. Still, most analysts of the industry and the doctors working the hospitals believe that the growth of one drug does not necessarily have to be the thing that kills the other.

Supposedly, the view these doctors have is that the data doesn’t hold enough clinical merit to take market share away from the established Avastin.

Both of these medications were designed to target a specific type of therapy. They’re supposed to help in blocking the mechanisms that are responsible for the growth of the cells in a tumor. Avastin has long been seen as the primary medication of this type, with more than double the sales of its closest rival, Erbitux. Still, the two drugs do have a number of differences that kept them largely away from each other’s market shares. Avastin, if I’m recalling this right, was used in advanced colorectal cancer – with some patient using it for lung and breast cancer, too. Erbitux, up until now, was approved for use as a treatment for colon cancer of the last resort variety – which means that it could only be given to a patient if all else fails. Head and neck cancer are not alien to the drug, either.

Still, the information does prove interesting to look at. Data showed that patients with certain genetic triggers and mutations in their tumors did not react to Erbitux. Most of the patients don’t have the mutation in their tumors, and they showed remarkable levels of improvement in their colorectal cancer after being given the drug. Regulators in Europe are considering approving it, but only for patients that don’t have mutant tumors rampantly growing inside them.

Resource Box : Harvey Ong is a part-time researcher, with special interest in the occult, medical anomalies, herbal lore, and psychology. He is also employed as a writer- researcher, researching and writing articles about a variety of pain killers, muscle relaxants, sexual health medications, and psychoactive drugs.

Stem Cells Might Fix Neurological Problems In Children

The Catholic Church would have you think that anything involving these things would be tantamount to selling your soul, your children’s souls, and your children’s children’s souls to the devil himself. All for the price of a shiny nickel, at that. Medical science would have you thinking otherwise. Medical science claims that the cells might be the key to curing a number of conditions, and providing treatment for some of the most lethal conditions known to man. The science behind it is sound, but the Church is opposed to it because of the supposed price tag: human embryos.

Now, we’re not going to get ourselves into the ridiculous debate about whether or not an embryo is alive or is just a bunch of cells (I personally take the latter side, but that’s beside the point) here. We are, however, going to delve into the latest development along the scientific front of this argument, because let’s face it, even if stem cells cure cancer, the Church is going to stay the Church and renounce it as “the devil’s work,” like they’ve been doing to various scientific achievements since the Dark Ages.

The latest development involves sticking embryonic stem cells into the brains of mice. Why is this a major development, oh wise and all-knowing guru, you may ask? I’ll tell you, and I won’t even charge you $300 for it, like a certain group that claims to be a religion but is actually a sham. You see, scientists stuck a few of the cells into the brains of mice. Now, these injected mice were all suffering from a neurological condition that, oddly enough, is something that human children suffer from. Okay, the conditions are eerily similar, but they’re not exact replicas of one another. Anyway, that’s not the point. The point is this: the mice recovered.

That’s right, the mice recovered from debilitating neurological conditions that would have otherwise left them mentally handicapped for the rest of their lives. Well, as mentally handicapped as can be recognized in mice, at least. The fact that some of these mice recovered has put up a lot of hope for the same technique being used to fix similar conditions in human children. As soon as science works all the problems out and figures out why other lab rats ended up dead anyway.

The core idea of the treatment is fixing the defective wires running though the brain and spinal cord. This means that the broken ones will either need to be repaired or replaced. The human body is largely capable of regenerating any sort of cell, even brain cells and neurons. However, some conditions can make that task either too slow to do any good, or completely shut it down. Besides, a lot of damage can be done while the body is working to fix itself. The stem cells are triggered to become the appropriate cells to conduct repairs, which is generally a lot faster than waiting for the body to generate new cells on its own.

By:Harvey Ong