Medi-Tech
  • Home
  • Covid
  • Services
    • Sterilization Services
    • Disinfection and Sanitization Services
    • Microbial Swabbing & Testing Services
    • Biofilm Identification and Remediation Services
    • Odor Removal Services
    • Extended Anti-Microbial Surface Protection
  • About
  • Resources
    • Terms of Use / Privacy Policy
Medi-Tech

MEDI TECH

05Jul

Our Mission at Medi-Tech

July 5, 2017 MEDI TECH Uncategorized

Medi-Tech will bring to the table win-win strategies to ensure proactive domination. Working with Doctors and other medical offices to help their patients have a more seamless doctor-patient visit or interaction.

Medi-Tech, Inc. efficiently unleashes products and services information to all of our clients making sure all of our clients are aware of the value we are offering. We at Medi-Tech, Inc. quickly maximize timely deliveries for real-time quick results and to dramatically maintain profitable solutions without sacrificing functional solutions.

Completely synergize resource taxing relationships via premier niche markets. Professionally cultivate one-to-one customer service with robust ideas. Dynamically innovate resource-leveling customer service for state of the art customer service.

Read more
07Nov

Vitamin D guidelines may be changed following new study

November 7, 2016 MEDI TECH Uncategorized
Vitamin D deficiency is reaching “epidemic” proportions.
A new study finds that, contrary to popular belief, vitamin D-2 and D-3 do not have equal nutritional value. With vitamin D deficiency on the rise, the authors call for a rethink of official guidelines.

Vitamin D is a vital nutrient, helping the gut to absorb calcium while keeping calcium and phosphate at the right concentrations to support healthy bone growth and maintenance. Without adequate levels in the body, bones can become brittle and misshapen.

Low vitamin D levels have also been linked with a range of other conditions, including cardiovascular disease and cancer.

Vitamin D is not naturally present in many foods. Instead, the bulk of our requirement is synthesized in the skin after exposure to ultraviolet light from the sun.

Despite the importance of vitamin D, many people in the United States do not have sufficient levels in their bodies. For example, one study found that overall, more than 40 percent of the U.S. population were vitamin D deficient. So much so, that some authors have referred to vitamin D deficiency as a pandemic.

Furthermore, in one study published in 2009, only 3 percent of black people in their sample of thousands of U.S. individuals had the recommended vitamin D levels, representing a decrease of 9 percent over the previous 20 years.

For this reason, it is becoming increasingly important to understand how the vitamin works and to ensure that the right type of supplements are reaching individuals most at risk.

Not all vitamin D types are equal

There are two types of vitamin D, which are known as D-2 and D-3. The former is derived from plant sources, particularly fungi, while the latter comes from animal sources.

The two types of vitamin D are very similar, differing only in the structure of their side-chains, and it is generally accepted that both perform similarly well as a supplement. In fact, on the National Institutes of Health website, they write, “The two forms have traditionally been regarded as equivalent.”

Researchers from the University of Surrey in the United Kingdom recently set out to test whether or not this widely held belief is correct. They wanted to understand which of the two nutrients raises levels of vitamin D in the body most effectively.

The researchers measured vitamin D levels in 335 South Asian and white European women over two winter periods. They chose winter because, due to a reduction in sunlight exposure, vitamin D levels tend to be lower at this time.

The women were split into five groups: those consuming vitamin D-2 in a biscuit; those consuming vitamin D-3 in a biscuit; those consuming vitamin D-2 in a juice drink; those consuming vitamin D-3 in a juice drink; and those receiving a placebo.

The study found that vitamin D-3 was twice as effective at raising vitamin D levels in the body as vitamin D-2.

Participants who received the D-3 in a biscuit raised their levels of vitamin D by 74 percent, while those receiving the vitamin in juice saw a 75 percent increase. Those receiving D-2 had a 33 and 34 percent increase, respectively. The placebo group experienced a drop of 25 percent across the same period.

Changes to guidelines and products

These findings have implications for the medical community, of course, but they also impact the retail sector; many companies add vitamin D-2 to beverages and foods. Some may therefore now want to think their choices.

As lead author Dr. Laura Tripkovic says, “The importance of vitamin D in our bodies is not to be underestimated, but living in the U.K., it is very difficult to get sufficient levels of it from its natural source, the sun, so we know it has to be supplemented through our diet.” The same can be said for many parts of the U.S.

She continues, “[O]ur findings show that vitamin D-3 is twice as effective as D-2 in raising vitamin D levels in the body, which turns current thinking about the two types of vitamin D on its head.”

“Those who consume D-3 through fish, eggs, or vitamin D-3-containing supplements are twice as likely to raise their vitamin D status than when consuming vitamin D-2-rich foods, such as mushrooms, vitamin D-2-fortified bread, or vitamin D-2-containing supplements, helping to improve their long term health.”

– Dr. Laura Tripkovic

Vitamin D deficiency appears to be widespread, and, as more research is conducted, it becomes increasingly clearer that this nutritional deficit is having a significant impact on the health of the country overall. Studies such as this may play a role in improving awareness, and, eventually, reversing the trend.

Read more
06Sep

Gut microbes influence the body’s response to high fat diet

September 6, 2016 MEDI TECH Uncategorized
The results of a new study provide evidence that it could be possible to tailor diets to individual patients, based on the signature of their gut microbiome.
New research explains why the same high-fat diet affects people differently. The team found that they could predict which mice would gain more weight and develop glucose intolerance after switching to a high-fat diet by using gut microbe signatures that were present before the switch.

In a paper published in Cell Reports, researchers from Imperial College London in the United Kingdom and INSERM UMRS 1138 in Paris, France, among others, describe how they used genetically similar mice to show that gut microbes influence the body’s response to changes in diet and affect health.

If further research finds that the effect is also true of humans, the researchers believe that it could lead to doctors prescribing personalized diets for patients based on the unique composition of their gut flora.

“We know that our environment and genetics can influence our risk of obesity and disease, but the effects of these communities of bacteria living inside us are less well understood,” says study leader Dr. Marc-Emmanuel Dumas, a reader in transnational systems medicine at Imperial College London.

Gut microbiome, health, and diet

The human gut, which represents one of the largest interfaces between the body and the environment, is home to vast colonies of bacteria and other microbes that have co-evolved with their hosts over thousands of years to play a vital role in health and disease.

From the day we are born, our gut microbiome – that is, the collection of gut microbes and their genetic material – is not only helping to digest food and make vitamins, but it is also shaping our immune system and the way our body responds to agents of disease.

Scientists are also starting to uncover a vast and complex system through which gut microbes might influence human brain development and behavior through their metabolites, the chemical byproducts of their activity.

It has also been established that diet is one of the main factors in shaping the gut microbiome over the course of life.

Now, Dr. Dumas and colleagues also show that there could be an effect in the other direction: that the gut microbiome may determine how the body responds to diet.

Gut microbiome predicts diet effects

For their study, the researchers placed around 50 mice with similar genetic makeup on a high-fat diet and tracked changes in their health and behavior.

Before switching the mice to the high-fat diet, the team used magnetic resonance spectroscopy to screen urine samples from the animals for metabolites of their gut microbes. This yielded a “gut microbiome signature” for each animal.

The high-fat diet resulted in several changes in the mice, but not all of them were affected in the same way, despite the fact that they were genetically similar.

Some mice put on more weight than others, and some became less tolerant of glucose. Glucose intolerance is an early sign of diabetes. There were also some changes in behavior, such as in levels of anxiety and activity.

Analysis against the animals’ gut microbiome signatures showed that they were predictive of some of the changes. The team found that one metabolite in particular, called trimethylamine-N-oxide, was an accurate predictor of glucose intolerance.

Co-senior author Jeremy K. Nicholson, a professor and head of the Department of Surgery and Cancer at Imperial College London, explains that in early life, “we start off with very few bugs” and our microbiome enlarges as we acquire more microbes from our environment.

“This means that small differences in the local environment can result in a great diversity in terms of the microbiome,” he adds, as he sums up the research:

“This study is another fascinating example of the power of the microbiome to influence the host with respect to major health risks. It shows that value of a diet is determined not only by your genes, but also the genes of your gut microbes.”

Read more
06Jun

Plantar flexion: Function, anatomy, and injuries

June 6, 2016 MEDI TECH Uncategorized
Plantar flexion describes the extension of the ankle so that the foot points down and away from the leg.

When in a standing position, this would mean pointing the foot towards the floor.

Plantar flexion has a normal range of motion from about 20 to 50 degrees from the resting position.

In this article, we examine the activities in which plantar flexion may occur, the muscles behind it, and what happens when injuries occur to these muscles.

Contents of this article:

  1. Function of plantar flexion
  2. What controls plantar flexion?
  3. Injuries
  4. Treatment
  5. Preventing injuries

Function of plantar flexion

Woman walking on tiptoes on wooden beam.
Plantar flexion is a term that describes positioning the foot with the toes furthest down. Standing on tiptoes is an example of plantar flexion.

Many daily activities involve plantar flexion. One typical example is pressing the foot down on the gas pedal in a car.

Standing on the tips of the toes to reach a high shelf is also plantar flexion. Ballet dancers who dance on the tips of their toes (en pointe) have an extreme range of motion in their plantar flexion.

These are more noticeable forms of plantar flexion, but plantar flexion takes place with every step a human takes.

Daily activities that require plantar flexion include:

  • walking
  • running
  • swimming
  • biking
  • dancing
  • jumping

Nearly every sport will require the use of plantar flexion. As a result, athletes are often encouraged to care for their ankles and the surrounding muscles as much as possible.

What controls plantar flexion?

Plantar flexion seems like a simple act, but it requires an entire group of muscles and tendons in the leg and foot.

Most muscles are centered on the tibia (shin bone) and the fibula, which is a thinner bone that supports the tibia. Muscles also attach to the ankle and various bones in the foot.

Gastrocnemius

The gastrocnemius is a muscle that forms half of what is commonly called the calf muscle. It starts at the back of the knee and attaches to the Achilles tendon at the heel.

The gastrocnemius is one of the muscles that does most of the work in plantar flexion.

Soleus

This is a broad and strong muscle that also starts behind the knee and runs beneath the gastrocnemius. It merges into the gastrocnemius to create the Achilles tendon at the heel.

The soleus muscle is responsible for pushing away from the ground. It is vitally important for any movement involving plantar flexion.

Plantaris

The plantaris muscle starts behind the knee, just above the gastrocnemius. The plantaris tendon runs below both the soleus and gastrocnemius muscles to connect directly with the heel bone.

This muscle works with the Achilles tendon to flex both the ankle and knee joints, allowing a person to stand on their toes or point their foot in plantar flexion.

Flexor hallucis longus

This is one of the three deep muscles of the leg. It starts along the back of the fibula and goes through the ankle, running along the sole of the foot to attach to the big toe.

The flexis hallucis longus helps plantar flexion of the ankle, and plays a large role in curling the toes. It is very important for walking and balancing, especially while on tiptoe.

Flexor digitorum longus

This is another deep muscle in the leg. The flexor digitorium longus starts on the back of the tibia near the soleus muscle. The muscle fibers end in a tendon that travels through the ankle and runs along the bottom of the foot.

The flexor digitorium longus attaches to every toe except the big toe. It is this muscle that provides the power to flex the toes themselves. It helps to support the arch of the foot and is used in plantar flexion.

Tibialis posterior

The tibialis posterior is the third deep muscle in the leg. It is the most central leg muscle and is vital in keeping the lower leg stable.

It is attached to interosseous membrane (which separates all bones) in the leg and is connected to the tibia and fibula. The tendon of the tibialis posterior spreads out to attach to the metatarsals, which are the five long bones in the top of the foot. The tibialis posterior is also attached to other bones in the foot – the medial cuneiform, middle and lateral cuneiform, and navicular bones.

Peroneus longus

Peroneus brevis.
The peroneus brevis ensures the foot is stable and any injury may weaken the ability to perform plantar flexion.

The peroneus longus muscle starts at the upper section of the fibula. It runs down most of the fibula bone and attaches to the medial cuneiform and first metatarsal, which are the bones below the large “knuckle” of the big toe.

The tibialis posterior and the peroneus longus work together in the middle foot to create support for the weight-bearing arches of the foot. These two muscles help keep the ankle stable when standing or rising onto the toes.

Peroneus brevis

The peroneus brevis lies just underneath the peroneus longus. It starts in the shaft of the fibula, and the tendon stretches to the foot, where it attaches to the metatarsal of the little toe. The peroneus longus and peroneus brevis help keep the foot stable.

All these muscles and tendons work together in plantar flexion to help the body stay balanced and stable. When there is a problem with even one of these muscles or tendons, the whole system is weakened, causing injury and a reduced range of motion.

Injuries

An injury to any one of the muscles supporting the act of plantar flexion will limit the range of motion of the foot. Ankle injuries are one of the most common ways to severely limit plantar flexion.

The ankle is a very complex joint. It is capable of a wide range of movement to stabilize the body in the most difficult situations, such as hiking or jumping on uneven surfaces. It does this while also protecting key ligaments, arteries, and nerves.

When the ankle is injured, inflammation helps prevent additional injury by reducing the range of motion of the foot. This can drastically reduce plantar flexion, sometimes to the degree where a person cannot move their foot.

Ankle injuries can range in severity from mild sprains to severe fractures. The severity of the injury will determine the treatment.

Treatment

Woman holding an ice compress on her ankle.
Injuries affecting plantar flexion can be treated using ice and compression.

Treating injuries depends on the type of injury that the person has sustained. Mild ankle sprains do not require casts or splints. Instead, they can be treated with rest, ice, compression, and elevation, known as the RICE method.

More severe sprains, tendon injuries, and some fractures will require a splint or cast to hold the ankle in its proper position. During this time, an individual will not be able to put weight on their foot or ankle.

If the ankle is not stable where the fracture has occurred, surgery is usually required. This may mean putting a plate or screws into the bones of the ankle to keep it in position while it heals. It usually takes a minimum of 6 weeks for a fracture to heal.

All forms of ankle, leg, or foot injury that affect plantar flexion will involve physical therapy and exercise to strengthen the muscles and tendons and protect them from future injury. Failing to do these exercises puts people at risk of further injuries in the future.

Preventing injuries

Preventing injuries in the muscles and joints that control plantar flexion starts with doing regular mobility and strength work. There are many exercises that can be done to strengthen the muscles and tendons that are used in plantar flexion and help protect the ankle.

Simple exercises such as toe raises can build strength. Low impact exercise such as swimming and biking can also promote flexibility and strength in the legs, feet, and ankles.

Stepping correctly can also help prevent injuries. Incorrect walking patterns may contribute to injuries over time. This can include walking in high heels or poorly fitted shoes.

Taking conscious steps can help if a person has a tendency to over correct or step incorrectly. It can also help to walk barefoot for at least 30 minutes each day, to allow the feet to walk in their natural position.

An appointment with a podiatrist or orthopedic surgeon may help anyone with regular injuries or limited plantar flexion to find a solution. This may help the doctor understand a person’s walking pattern and decide whether they would benefit from particular shoes or specific exercises.

Read more
06May

Breast cancer: Maternal high-fat diet raises risk across generations

May 6, 2016 MEDI TECH Uncategorized
Researchers have found that a high-fat diet may raise the risk of breast cancer across generations.
New research conducted on pregnant female mice shows that exposure to a high-fat diet can increase the risk of breast cancer across generations. These findings may consolidate understanding of breast cancer factors and help to improve prevention.

Breast cancer is the second most widespread type of cancer among women in the United States, according to the American Cancer Society (ACS), who estimate that there will be around 40,610 deaths attributed to this type of cancer in 2017.

The known causes of lifestyle-related breast cancer have so far included alcohol consumption, lack of physical exercise, obesity, choice of contraceptives, hormone therapy, and breast-feeding. The new research may add an imbalanced diet during pregnancy to this list.

A new study carried out by the Georgetown Lombardi Comprehensive Cancer Center in Washington, D.C., suggests that eating foods that are high in fat during pregnancy may affect the risk of developing breast cancer in female offspring across generations.

Senior study author Leena Hilakivi-Clarke, Ph.D., a professor of oncology at Georgetown Lombardi, and colleagues recently reported their findings in the journal Breast Cancer Research.

Testing a high-fat diet in mice

To study the inter-generational impact of diet, the mice specimens were mated in two different phases. In the first phase of the experiment, the pregnant female mice were randomly divided into one of two groups after mating.

The females in the first group were fed a diet with a normal fat intake, with 16 percent of its calories taken from fat, while those in the second group were fed a high-fat diet.

The high-fat diet took just over 41 percent of its calories from fat. Around 39 percent of these calories came from corn oil, while roughly 2 percent of the calories came from soybean oil.

Since the gestation period in mice is around 19 to 21 days, the controlled feeding of the second group started on day 10 of their pregnancy, which roughly corresponds to the second trimester of pregnancy in humans, a point at which the ovaries of the female fetus begin to develop.

The offspring and further generations that resulted from this phase of the experiment were placed on a normal diet.

High-fat diet caused genetic changes

In the second phase of the experiment, the female offspring that resulted from the previous phase (first-generation offspring) were mated with males fed a high-fat diet. All the females that fell pregnant in this stage were fed a normal diet.

It was observed that first- and third-generation female offspring, or daughters and great-granddaughters, that had been exposed to a high-fat diet through their mothers were at an increased risk of developing breast cancer, and that malignant tumors settled earlier in these generations.

Some differences in the genetic structure of first- and third-generation offspring were also found. Tests revealed that third-generation female mice presented three times more changes in the genetic makeup of their mammary glands when compared with first-generation female mice.

This finding suggests that direct exposure in the womb to a genetic makeup already susceptible to an increased threat of malign tumors amplifies the risk of breast cancer development over generations.

“The soil in the breast, so to speak, remained fertile for breast cancer development in our high-fat experimental mice,” says Prof. Hilakivi-Clarke.

Implications for breast cancer

“Studies have shown that pregnant women consume more fats than non-pregnant women, and the increase takes place between the first and second trimester,” adds Prof. Hilakivi-Clarke.

This knowledge, combined with the results of the study, suggests that more attention should be paid to women’s intake of fatty foods during pregnancy, in light of the potential links between gestational diet and the risk of breast cancer in future generations.

According to the ACS, there are currently more than 3.1 million breast cancer survivors in the U.S. Risk factors and prevent-ability are often a point of contention among specialists. Some factors, such as induced abortion, have been disproved, while others, including smoking, are still being considered.

Studies such as this provide hope that prevent-ability, as well as the survivor ratio, will increase with time, as specialists gain a better understanding of the advertible causes of breast cancer.

Read more
07Apr

Antioxidant suppression eradicates pancreatic cancer cells

April 7, 2016 MEDI TECH Uncategorized
A novel drug therapy – that mimics the suppression of an antioxidant-promoting protein – kills pancreatic cancer cells, new research reveals.
A reduction of antioxidants in pancreatic cancer cells can help kill them.

According to the American Cancer Society, around 53,070 people will be diagnosed with pancreatic cancer in the Unites States in 2016, and around 41,780 people will die of the disease. Pancreatic cancer accounts for about 3 percent of all cancers in the U.S. and about 7% of cancer deaths.

Pancreatic cancer is caused by the abnormal, uncontrolled growth of cells in the pancreas.

A research team at Cold Spring Harbor Laboratory (CSHL) in New York finds that reducing levels of antioxidants in pancreatic cells can help to kill them. This new strategy for eradicating pancreatic cancer cells may open new doors for treating this serious illness, in which less than 5 percent of patients survive 5 years.

“Antioxidant” has become a popular buzzword that is viewed as a cure-all notion for health ailments; it is widely believed that raising levels of antioxidants stops cancer cells from developing.

In reality, although antioxidants interact with and neutralize free radicals and prevent them from causing damage, there is little available evidence that antioxidants prevent cancer.

Furthermore, trials have found that people taking antioxidant supplements during cancer therapy have worse outcomes, especially if they were smokers.

Does increasing antioxidant levels do more harm than good?

In a series of complex experiments, the CSHL researchers demonstrate that in pancreatic cells that are abnormal or in a malignant state, raising antioxidant levels can do more harm than good.

In healthy cells, the amounts of oxidizing and anti-oxidizing agents are kept precisely balanced in every cell.

However, in proliferating cancer cells – that are increasing rapidly in number through growth and cell division – the amounts of oxidants in malignant cells increase, but anti-oxidants also increase to counter the impact of rising oxidation.

CSHL’s Prof. David Tuveson – M.D., Ph.D., director of research for the Lustgarten Foundation – and colleagues note that without the amounts of antioxidants going up in scale with the oxidants, malignant cells will die from excessive oxidation.

“Of course, that’s exactly what we want cancer cells to do – to burn themselves out,” says Iok In Christine Chio, a postdoctoral investigator in the Tuveson lab who led the experiments.

“The therapeutic principle our lab is testing is whether, by increasing the level of oxidation in cancer cells, we can cause pre-malignant and malignant cells to die,” she adds.

Excessive oxidation causes cells to commit suicide

Treatments for cancer such as radiation therapy and chemotherapy destroy cancer cells by promoting oxidation. Although antioxidants protect cellular DNA from damage by oxidation stress, they likely protect cancer cells, too.

Exposing cells to excessive oxidation causes them to experience programmed cell death called apoptosis. A method of increasing oxidation in cancer cells is to decrease levels of antioxidants within the same cells.

Tuveson and team aimed to find a technique whereby they could increase oxidation without harming healthy cells. They concentrated on NRF2, a protein that can be tweaked to disrupt the balance between oxidation and decreased cancer cells.

When NRF2 is active, cells synthesize a chemical called glutathione, an important antioxidant. However, it is not possible to reduce NRF2 activity or make it inactive, as it has a role in regulating several hundred different genes. “One can’t delete it from a cell without impacting many other processes,” says Chio.

The team used samples of pancreas cells from people with pancreatic cancer (malignant and pre-malignant) and individuals with a healthy pancreas to conduct an experiment where NRF2 was eliminated.

Normal pancreas cells not harmed by two-drug treatment

They found that when NRF2 was missing, the process of translating messages from the genes into proteins was highly affected by the oxidant and antioxidant balance, but only in the cancerous cells. The healthy cells were still able to produce the proteins.

“We were very excited when we saw this. This meant that if we could find a way of reducing antioxidants, protein synthesis would only be impacted in precancerous and malignant cells, a potentially powerful therapeutic strategy.”

Iok In Christine Chio, postdoctoral investigator, Tuveson Lab

The crux of the experiment was to use two drugs in combination: an AKT (protein kinase B) inhibitor, and a BSO (buthionine sulfoximine), which reduces levels of glutathione.

AKT inhibitors have been used in trials on cancer patients before but with limited success. The team wanted to combine this with the BSO to mimic what would happen if they could reduce levels of NRF2.

“We were able to test this idea and see that this approach was synthetically lethal – it did increase the killing power of the AKT inhibitor, but the synergy was not present in the setting of normal pancreas cells,” Chio says. Fundamentally, healthy pancreas cells were not damaged by the treatment.

The team hopes their findings can enable them to propose new treatments and approaches for cancer patients, and they hope to start clinical trials in the near future.

Read more
06Apr

Why do chili peppers give us the hiccups?

April 6, 2016 MEDI TECH Uncategorized
Chili peppers leave some people cool, but they can give others the hiccups.
If you love spicy food, then you’ve probably experienced the intense – and sometimes quite uncomfortable – chili hiccups. But what causes this phenomenon, and why are some chili-lovers more affected than others?

Chili peppers contain a chemical compound called capsaicin, which is part of a group of chemicals that give chilies their individual taste and heat profile. Capsaicin can activate neurons in the diaphragm, which contracts and causes hiccups.

Capsaicin is also an irritant. Chili plants are thought to use capsaicin as a defense mechanism in order to stop animals from eating the plant. In fact, humans are the only species known to enjoy eating spicy food.

Chili peppers and pain

Capsaicin binds to a pain receptor called TRPV1. When we accidentally expose our skin or eyes to chilies, we activate TRPV1 receptors, thereby causing the pain floodgates open. These receptors in our mouths are the reason for the “mouth-on-fire” feeling we experience when we eat spicy food.

Interestingly, once a pain receptor is stimulated by capsaicin, it goes into a period of rest, which means that the same receptor doesn’t transmit pain signals again.

Scientists call this process “defunctionalization.” This is why capsaicin is used to treat pain in some patients; it leads to loss of pain perception.

The capsaicin receptor is found throughout the body, including in the nerves that control our diaphragm, which is the muscle that allows our lungs to take in air.

Hiccups are thought to be caused by an involuntary contraction, or spasm, of the diaphragm, followed by contraction of the glottis. Airflow into the windpipe becomes temporarily blocked. When incoming air strikes the glottis, the characteristic hiccup sound occurs.

Scientists are still speculating about the precise mechanism responsible for hiccups, as well as how exactly capsaicin leads to spasms of the diaphragm, which, at this point, remains unclear.

Luckily, the capsaicin molecules that we eat in food don’t stick around for very long; they are rapidly absorbed in the stomach and intestine to be broken down.

But why do some of us start to hiccup at the mere sight of a chili, while others don’t seem to be bothered by spicy foods at all?

Nature, nurture, and the chili response

A Finnish study showed that our preference for spicy food is partly determined by our genes. Differences in number and distribution of capsaicin receptors in our mouths also contribute to our responsiveness to spicy food.

It is, of course, possible to build up a tolerance to chili peppers. There are no definitive scientific studies on human subjects yet, but we can speculate that the mechanism of tolerance occurs through repeated exposure to capsaicin. This will defunctionalize the TRPV1 receptors in the mouth, allowing us to get used to eating spicier food.

Read more
06Apr

Immune cells in the brain may cause weight gain

April 6, 2016 MEDI TECH Uncategorized
The results of a new study suggest that immune cells in the brain called microglia could become treatment targets for obesity.
New research suggests that microglia, which are brain-resident immune cells, may offer a new target for obesity treatments. In mice, the scientists found that fat-rich diets cause microglia to trigger overeating and weight gain.

A paper on the work – led by the University of California-San Francisco (UCSF) and the University of Washington Medical Center in Seattle – is published in the journal Cell Metabolism.

The researchers believe that the discovery may lead to new obesity drugs that avoid many of the side effects associated with those currently approved for clinical use.

Co-senior author Suneil Koliwad, an assistant professor of medicine at the UCSF Diabetes Center, says that their findings suggest that microglia might be “an untapped and completely novel way to target the brain in order to potentially mitigate obesity and its health consequences.”

Microglia account for 10 to 15 percent of the cells in the brain and spinal cord. They are not the same as neurons, which are brain cells that communicate with each other using electrical and chemical signals.

Microglia are immune cells that play an important role in brain infection and inflammation.

Scientists are beginning to discover that these cells are highly active, even in the resting healthy brain. They are in constant motion, carrying out surveillance and triggering a wide range of responses.

High-fat diets increase microglia

It is coming to light that microglia also influence brain circuit activity during normal conditions. For example, during brain development, they help to shape brain circuits that are important for behavior and response to disease. In the mature brain, they can influence the activity of neurons.

It was already known that a group of neurons in the mediobasal hypothalamus help to regulate the amount of food we eat and how much energy we use.

Under normal conditions, this portion of the brain tries to balance our energy needs with the amount of calories we ingest from food and keep our weight healthy. However, researchers have discovered that eating fat-rich foods can disrupt this balancing process.

Previous research has shown that mice fed fat-rich diets eat more, burn fewer calories, and put on more weight than equivalent mice fed low-fat diets. Fat-rich diets also increase the number of microglia and inflammation in the mice’s mediobasal hypothalamus.

Prof. Koliwad and colleagues wanted to find out whether it is the increase in microglia that causes the overeating and weight gain, or whether it is the weight gain that increases the number of microglia.

Microglia-induced inflammation

The researchers ran an experiment wherein they put two groups of mice on a fast-food, fat-rich diet for 4 weeks. At the same time, one group of mice was treated with a drug that reduced the microglia in their mediobasal hypothalamus, while the other was not.

The results showed that the mice treated with microglia-reducing drug ate 15 percent less food and put on 20 percent less weight than the untreated group fed the same fatty diet.

This suggested that it was the increase in microglia that caused overeating and weight gain. However, it was still not clear whether or not this was due to the microglia triggering inflammation. Thus, the researchers conducted further experiments to find out.

They genetically engineered mice so that their microglia could not trigger immune responses. When fed the fatty diet, these mice ate 15 percent less food and gained 40 percent less weight than normal mice. This suggested that it was the ability of the microglia to trigger inflammation that caused it.

The researchers confirmed this in another group of mice that had been genetically engineered so that their microglia triggered inflammation in response to a drug.

They found that even when these mice were fed a healthful, low-fat diet, giving them the drug triggered their microglia to induce inflammation in the hypothalamus. This caused the treated mice to eat 33 percent more food, use 12 percent less energy, and put on four times more weight than untreated mice on the same diet.

Similar drug already in human trials

The authors note that a drug currently undergoing human trials for the treatment of leukemia, other cancers, and arthritis acts in the same way as the drug that they used to reduce microglia in the mice. They are watching with interest to see if the drug causes the patients in the trials to lose weight.

The team also discovered that when the mice were fed the fat-rich diet, their microglia recruited extra immune cells from the bloodstream.

These blood-borne immune cells not only joined their cousins in the hypothalamus, but they also underwent changes that made them act in a similar way, increasing their inflammation response as well as their influence on energy balance.

The researchers say this suggests that there might be more than one way to influence the microglia to prevent weight gain: through one target in the brain and another target in the bloodstream.

Recent imaging studies show that, compared with slim people, obese people are more likely to have increased numbers of glial cells – the class that microglia belong to – in their hypothalamus. This localized increase of glial cells, called gliosis, is often seen in brain trauma, brain infection, brain cancer, and neurodegenerative diseases.

Ancient survival advantage

Speculating on why glia and microglia might behave in this way, Prof. Koliwad says that the answer might lie in evolution. Perhaps the response is an ancient survival mechanism that was effective in an era wherein energy-rich food was scarce, ensuring that people stored up reserves for leaner times by increasing their appetite.

“Microglial responsiveness to dietary fats makes some sense from this evolutionary perspective. Fats are the densest form of calories that ancient humans might ever [have] had the opportunity to consume,” he explains.

But in today’s modern world, in which high-fat foods are constantly available, the ancient survival advantage has become a disadvantage that can harm rather than preserve life.

Modern humans are more likely to overeat high-fat foods all the time, rather than once in a while. This causes the microglia trigger to be permanently on, leading to increased appetite and a vicious cycle of increasing intake of high-fat food.

The team now plans to investigate in more detail the mechanism through which eating fat-rich foods activates the microglia.

“From these experiments, we can confidently say that the inflammatory activation of microglia is not only necessary for high-fat diets to induce obesity, but also sufficient on its own to drive the hypothalamus to alter its regulation of energy balance, leading to excess weight gain.”

Co-senior author Prof. Joshua Thaler, University of Washington Medical Center

Read more
07Mar

Parts of Mediterranean diet shown to prevent colorectal cancer

March 7, 2016 MEDI TECH Uncategorized
New research singles out a few key elements of the Mediterranean diet that are most important for colorectal health.
The benefits of the so-called Mediterranean diet have been hailed in the news over recent years. Now, new research looks closely at the elements of the diet that could help to prevent the risk of colorectal cancer.

Among many other benefits, the Mediterranean diet has been shown to lower the risk of colorectal cancer. But the specifics of this beneficial role have not been studied in depth.

New research – presented at the ESMO 19th World Congress on Gastrointestinal Cancer, held in Barcelona, Spain – singles out the few components of the Mediterranean diet key for preventing colorectal cancer. The first author of the study is Naomi Fliss Isakov, Ph.D., of the Tel-Aviv Medical Center in Israel.

More specifically, the research looks at the link between the components of the diet taken both separately and in combination, as well as the risk of developing advanced colorectal polyps.

Colorectal cancer tends to develop from advanced polyps, or adenoma. However, the chances of polyps becoming malignant depend on various factors, including size, structure, and location.

Zooming in on the Mediterranean diet

Dr. Isakov and team examined 808 people who were undergoing either screening or diagnostic colonoscopies.

The participants were aged between 40 and 70 years old and were not at a high risk of colorectal cancer. The researchers took anthropometric measurements – such as body mass index (BMI) and height – of the participants, and they asked them to fill in a food frequency questionnaire. They also took part in a medical and lifestyle interview.

The researchers defined adherence to the Mediterranean diet as an above-average consumption of fruit, vegetables, nuts, seeds, and whole grains, as well as fish and poultry.

A below-median intake of red meat, alcohol, and soft drinks was also considered to be a key component of the diet. A Mediterranean diet was also described as having “a high ratio of monounsaturated to saturated fatty acids.”

For the purposes of the study, the researchers defined advanced polyps as adenomas larger than 10 millimeters in size, with a “high-grade dysplasia or villous histology.”

As the American Cancer Society (ACS) explain, the term “dysplasia” refers to the abnormal aspect of the polyps. “High-grade dysplasia” is a term used to describe polyps that appear abnormal or cancer-like. The ACS also note that larger adenomas tend to have a villous growth pattern and are more likely to lead to cancer.

Dr. Isakov and colleagues also examined healthy controls who did not have any polyps, either in the past or at the time of the study.

More fish, fruit reduces risk

Having compared individuals with polyp-free colonoscopies and those whose colonoscopy showed advanced polyps, the authors found a clear association between components of the Mediterranean diet and the risk of colorectal cancer.

People with advanced polyps reported consuming fewer elements of the Mediterranean diet. More specifically, the average was 1.9 Mediterranean diet components in the advanced polyps group, compared with 4.5 components in the polyp-free group.

Surprisingly, even two or three elements of the diet correlated with a 50 percent reduction in the risk of advanced polyps, compared with consuming no key components at all.

Additionally, the risk further decreased as the number of Mediterranean elements increased. The more elements of the Mediterranean diet people consumed, the lower were the chances of advanced polyps showing up in their colonoscopies.

The researchers adjusted for other risk factors associated with colorectal cancer and found that increased fish and fruit consumption, together with a low intake of soft drinks, was most likely to reduce the risk of advanced polyps.

“We found that each one of these three choices was associated with a little more than 30 percent reduced odds of a person having an advanced, pre-cancerous colorectal lesion, compared to people who did not eat any of the MD [Mediterranean diet] components.”

Naomi Fliss Isakov, Ph.D.

She concluded, “Among people who made all three healthy choices the benefit was compounded to almost 86 percent reduced odds.”

ESMO spokesperson Dr. Dirk Arnold, of the Instituto CUF de Oncologia in Lisbon, Portugal, also comments on the findings, saying, “This large population-based cohort-control study impressively confirms the hypothesis of an association of colorectal polyps with diets and other lifestyle factors.”

“This stands in line with other very recent findings on nutritive effects, such as the potential protective effects of nut consumption and vitamin D supplementation which have been shown earlier this year.”

“However,” adds Dr. Arnold, “it remains to be seen whether these results are associated with reduced mortality, and it is also unclear if, and when a dietary change would be beneficial.”

Next, the authors plan to investigate the effects of the Mediterranean diet in a group at high risk of developing colorectal cancer.

Read more
06Feb

New study explains how low-dose aspirin may prevent cancer

February 6, 2016 MEDI TECH Uncategorized
Cancer is a leading cause of morbidity and death worldwide, and its prevalence is predicted to increase in the next few years. Cancer prevention strategies include making healthy lifestyle choices and getting tested if at risk. New research suggests that a small dose of aspirin may help prevent the formation of cancer cells and explains how.
[pills spilling out of a bottle of aspirin]
New research explains how ‘baby’ aspirin may help to prevent cancer.

According to the World Health Organization (WHO), cancer is one of the leading causes of death across the globe, accounting for 8.2 million deaths in 2012.

In terms of prevention, the Centers for Disease Control and Prevention (CDC) recommend making healthy lifestyle and dietary choices, such as avoiding tobacco and alcohol, as well as staying physically active and eating plenty of fruits and vegetables.

New research reinforces the idea that low-dose aspirin intake may also help to prevent cancer and inhibit the proliferation of cancer cells.

The suggestion that a small dose of aspirin may help to prevent cancer is not new. In September 2015, the United States Preventive Services Task Force recommended the daily use of a small dose of aspirin to help to prevent cardiovascular disease and colorectal cancer.

However, the new research also explains the process by which a low dose of aspirin may indeed inhibit cancer cell proliferation and metastasis.

Aspirin indirectly inhibits oncoprotein responsible for malignant cells

The research was conducted by scientists from Oregon Health and Science University (OHSU) in collaboration with Oregon State University (OSU), and the results were published in the journalAJP-Cell Physiology.

“The benefit of aspirin may be due to its effect on blood cells called platelets, rather than acting directly on tumor cells,” says senior author Owen McCarty, a professor in the Department of Biomedical Engineering at OHSU.

Platelets are tiny blood cells that help a healthy body to form clots, in order to stop the bleeding when necessary.

It seems that our blood platelets also increase the levels of a certain protein that may support cancer cells and help them to spread. This “oncoprotein” is called c-MYC.

The biological function of c-MYC is to regulate the expression of over 15 percent of all the genes of the human body. The c-MYC regulator controls the life-and-death cycle of cells, the synthesis of proteins, and the cells’ metabolism.

However, research has shown that in human cancers, this oncogene is overexpressed.

The researchers from this latest study explain that aspirin reduces the ability of blood platelets to raise levels of the c-MYC oncoprotein.

“Our work suggests that the anti-cancer action of aspirin might be in part as follows: during their transit in the blood, circulating tumor cells interact with platelets, which spur tumor cell survival by activating oncoproteins such as c-MYC. The inhibition of platelets with aspirin therapy reduces this signaling between platelets and tumor cells, thus indirectly reducing tumor cell growth.”

Owen McCarty

Craig Williams, a professor in the OSU/OHSU College of Pharmacy and co-author of the study, further explains the process.

“Early cancer cells live in what is actually a pretty hostile environment, where the immune system regularly attacks and attempts to eliminate them,” he says. “Blood platelets can play a protective role for those early cancer cells and aid metastasis. Inhibition with aspirin appears to interfere with that process and c-MYC may explain part of that mechanism.”

Low-dose aspirin may be ‘safe and efficacious’ in preventing cancer

This is the first time that a study has shown the ability of platelets to regulate the expression of c-MYC in cancer cells.

The researchers note that almost a third of colon cancer patients and 42 percent of patients with pancreatic cancer had overexpression of the c-MYC oncoprotein.

They also point out that the impact aspirin has on blood platelets is just as effective in high doses as it is at low ones. As a result, clinicians can weigh up the risks and benefits of aspirin intake, as well as reduce the risk of bleeding – which is a common side effect of ingesting too much aspirin.

The authors emphasize the crucial role of physicians and healthcare professionals when considering even a low-dose aspirin intake.

“Because the interaction between platelets and cancer cells is believed to occur early […] the use of anti-platelet doses of aspirin might serve as a safe and efficacious preventive measure for patients at risk for cancer,” the authors conclude.

Read more
    12