Meditation benefits the Brain ?

Experienced meditators seem to be able switch off areas of the brain associated with daydreaming as well as psychiatric disorders such as autism and schizophrenia, according to a new brain imaging study by Yale researchers.

Meditation's ability to help people stay focused on the moment has been associated with increased happiness levels, said Judson A. Brewer, assistant professor of psychiatry and lead author of the study published the week of Nov. 21 in the Proceedings of the National Academy of Sciences. Understanding how meditation works will aid investigation into a host of diseases, he said.

"Meditation has been shown to help in variety of health problems, such as helping people quit smoking, cope with cancer, and even prevent psoriasis," Brewer said.

The Yale team conducted functional magnetic resonance imaging scans on both experienced and novice meditators as they practiced three different meditation techniques.

They found that experienced meditators had decreased activity in areas of the brain called the default mode network, which has been implicated in lapses of attention and disorders such as anxiety, attention deficit and hyperactivity disorder, and even the buildup of beta amyloid plaques in Alzheimer's disease. The decrease in activity in this network, consisting of the medial prefrontal and posterior cingulate cortex, was seen in experienced meditators regardless of the type of meditation they were doing.

The scans also showed that when the default mode network was active, brain regions associated with self-monitoring and cognitive control were co-activated in experienced meditators but not novices. This may indicate that meditators are constantly monitoring and suppressing the emergence of "me" thoughts, or mind-wandering. In pathological forms, these states are associated with diseases such as autism and schizophrenia.

The meditators did this both during meditation, and also when just resting - not being told to do anything in particular. This may indicate that meditators have developed a "new" default mode in which there is more present-centered awareness, and less "self"-centered, say the researchers.

"Meditation's ability to help people stay in the moment has been part of philosophical and contemplative practices for thousands of years," Brewer said. "Conversely, the hallmarks of many forms of mental illness is a preoccupation with one's own thoughts, a condition meditation seems to affect. This gives us some nice cues as to the neural mechanisms of how it might be working clinically."

Ischemia

Ischemia symptoms can vary based on where in the body the condition occurs, and many times no
symptoms are present until a health complication arises. Chest pain, shortness of breath, and heaviness in the chest can be potential symptoms of ischemia occurring at the heart muscle. Bowel ischemia can cause digestive upset and discomfort, while dizziness, confusion, and dementia can occur in the brain. These symptoms can be severe or minor, although they generally worsen if not treated promptly.

Ischemia is a condition which is characterized by a lack of blood flow to a particular organ or system of the body, which often results in tissue damage. There are both reversible and irreversible varieties of this condition, and there are a number of potential causes and treatments. Sometimes tissue damage is so severe it cannot be fully corrected.

What is a Cardiopathy

Cardiopathy is a medical term that can refer to several different types of heart disease. The condition can involve the weakening of the heart muscle, a structural abnormality, or a blockage that affects the heart's ability to pump blood throughout the body. Cardiopathy can arise because of inherited and congenital disorders, unhealthy lifestyle choices, and acquired medical conditions like high blood pressure. Without an accurate diagnosis and treatment, heart disease is usually fatal. There are many different medical and treatment options, however, that can improve a person's chances of overcoming cardiopathy.

Heart disease may be caused by a number of different factors. Some defects are present at birth, while other conditions do not arise until later in life. Consuming excessive amounts of alcohol, smoking, and eating unhealthy foods greatly increases the risk of developing high blood pressure and atherosclerosis, a condition in which arteries become blocked with buildups of hardened cholesterol. Arterial blockages are a leading cause of heart problems because blood cannot be efficiently pumped through the heart. Cardiomyopathy is another common form of heart disease in which the heart muscle is weakened and thereby inhibited from functioning properly.

Acne

Acne is a pustular infection of the skin, caused by changes in the sebaceous glands. Excessive secretion of oils from the glands combine with naturally occurring dead skin cells to block the hair follicles. Oil secretions build up beneath the blocked pore, providing a perfect environment for the skin bacteria Propionibacterium acnes to multiply uncontrolled. In response, the skin inflames, producing the visible lesion. The face, chest, back and upper arms are especially exposed.

The infection is common in puberty as a result of an abnormal response to normal levels of the male hormone testosterone. The response for most people diminishes over time and acne thus tends to disappear, or at least decrease, after one reaches early adulthood. There is, however, no way to predict how long it will take for it to disappear entirely, and some individuals will continue to suffer from acne decades later, into their thirties and forties and even beyond.

Alzheimer's disease

Alzheimer's disease (AD) is the most common cause of dementia in western countries. Approximately 10% of all persons over the age of 70 have significant memory loss; in more than half the cause is AD. AD is a progressive dementia (that is the dementia keeps getting worse).

In the early stages of the disease, the memory loss may go unrecognized or may be ascribed to benign forgetfulness. Slowly the cognitive problems begin to interfere with daily activities, such as keeping track of finances, following instructions on the job, driving, shopping, and housekeeping. Some patients are unaware of these difficulties (agnosognosia), and others have considerable insight, resulting in frustration and anxiety. These major differences in insight have no clear explanation.

The most important risk factors for AD are old age and a positive family history. The frequency of AD increases with each decade of adult life to reach 20 to 40% of the population over the age of 85. A positive family history of dementia suggests a genetic cause of AD.

Too Little Salt Can Also Be A Problem

We've been bombarded for more than two decades with scientists and doctors telling us to eat less salt. Statistics show that those eating excessive salt in their diets are far more likely to suffer from cardiovascular problems, but as with any nutritional or diet information, moderation and balance is the key. Everyone is familiar with the active salt intake in hot countries like Mexico and Spain, where more salt is lost through perspiration, so it should come as no surprise that too little salt can also be a problem.

A study in the November 23 issue of JAMA shows that too high or too low sodium levels in urine carries a far higher risk for cardiovascular events (for higher levels), or cardiovascular death and hospitalization for congestive heart failure for lower levels.

Researchers also found higher estimated urinary potassium excretion was associated with a reduced risk of stroke.

The exact daily recommended salt intake is still not precisely clear, and would be an academic number, since it would be fairly difficult for the average person to accurately measure how much salt they eat on a day to day basis. A lot would also depend on the climate they live in and how active they are.

Researchers say that :

"Clarifying the optimal daily intake of sodium is particularly important in patients with established Cardiovascular (CV) disease, where it has been inadequately studied. Patients with CV disease may be especially vulnerable to the CV effects of high and low sodium intake and are most likely to receive recommendations on restricting sodium intake."


The authors also note that the optimal level of daily potassium intake, a proposed modifier of the association between sodium intake and CV disease, has not been established.

Martin J. O'Donnell, M.B., Ph.D., and Salim Yusuf, D.Phil., F.R.C.P.C., F.R.S.C., of McMaster University, Hamilton, Ontario, Canada, and colleagues examined the association between sodium and potassium excretion (markers of intake) and CV events and mortality.

The study consisted of an observational analyses of 2 cohorts (n = 28,880) included in the ONTARGET and TRANSCEND trials (November 2001-March 2008 from initial recruitment to final follow-up). The researchers estimated 24-hour urinary sodium and potassium excretion from a morning fasting urine sample. Multivariable models were used to determine the association of urinary sodium and potassium with CV events (myocardial infarction [MI; heart attack], stroke, and hospitalization for congestive heart failure (CHF) and mortality.

At study entry, the average estimated 24-hour excretion for sodium was 4.77 g and 2.19 g for potassium. After a median (midpoint) follow-up of 56 months, the composite outcome occurred in 4,729 (16.4 percent) participants. The researchers found that after multivariable analysis, compared with baseline sodium excretion of 4 to 5.99 g per day (n = 14,156 [15.2 percent with the composite outcome]), higher baseline sodium excretion (18.4 percent for 7-8 g/d and 24.1 percent for greater than 8 g/d) and lower sodium excretion (18.2 percent for 2-2.99 g/d and 20.2 percent for less than 2g/d) were associated with an increased risk of the composite of CV death, heart attack, stroke, and hospitalization for CHF.

Compared with the reference group, higher baseline sodium excretion was associated with an increased risk of CV death (9.7 percent for 7-8 g/day; and 11.2 percent for greater than 8 g/day), MI (6.8 percent for greater than 8 g/day), stroke (6.6 percent for greater than 8 g/day), and hospitalization for CHF (6.5 percent for greater than 8 g/day). Lower sodium excretion was associated with an increased risk of CV death (8.6 percent for 2-2.99 g/day; 10.6 percent for less than 2 g/day), and hospitalization for CHF (5.2 percent for 2-2.99 g/day) on multivariable analysis. Compared with an estimated potassium excretion of less than 1.5 g per day, higher potassium excretion was associated with a reduced risk of stroke on multivariable analysis.

The researchers conclude that :

"Discrepant findings of previous studies are likely due to differences in ranges of sodium intake, study populations, methods of measurement, and failure to explore a nonlinear association ... Compared with moderate sodium excretion, we found an association between high sodium excretion and CV events and low sodium excretion and CV death and hospitalization for CHF, which emphasizes the urgent need to establish a safe range for sodium intake in randomized controlled trials.

Higher urinary potassium excretion was associated with lower stroke risk and is a potential intervention that merits further evaluation for stroke prevention."


They also mention that previous individual prospective cohort studies have either reported a positive association, no association, or an inverse relationship between sodium intake and CV mortality, and that this area clearly needs further investigation.

What Is Heart Rate? What Is A Healthy Heart Rate?

A person's heart rate, also known as their pulse, refers to how many times their heart beats per minute. Our heart rates vary tremendously, depending on the demands we make on our bodies - a person who is sleeping will have a much lower heart rate compared to when he/she is doing exercise.

There is a technical difference between heart rate and pulse, although they both should come up with the same number:
Heart rate - how many times the heart beats in a unit of time, nearly always per minute. The number of contractions of the lower chambers of the heart (the ventricles).
Pulse (pulse rate) - as the blood gushes through the artery from a heart beat, it creates a bulge in the artery. The rate at which the artery bulges can be measured by touching it with your fingers, as on the wrist or neck.
According to Medilexicon's medical dictionary:

Heart beat is "A complete cardiac cycle, including spread of the electrical impulse and the consequent mechanical contraction."

Pulse is "Rhythmic dilation of an artery, produced by the increased volume of blood thrown into the vessel by the contraction of the heart. A pulse may also at times occur in a vein or a vascular organ, such as the liver."


Doctors and other healthcare professionals measure patients' heart rates when monitoring their health, gauging the effectiveness of certain treatments, or making a diagnosis.

Athletes and sports people usually measure their heart beats so that they can gain maximum efficiency from their training regimes.
What is a normal resting heart rate (pulse rate)?
For a human aged 18 or more years, a normal resting heart rate can be anything between 60 and 100 beats per minute. Usually the healthier or fitter you are, the lower your rate. A competitive athlete may have a resting heart rate as low as 40 beats per minute.

Champion cyclist, Lance Armstrong has had a resting heart rate of about 32 beats per minute (bpm). Fellow cyclist Miguel Indurain once had a resting heart rate of 29 bpm.

According to the National Health Service, UK, the following are ideal normal pulse rates at rest, in bpm (beats per minute):
Newborn baby - 120 to 160
Baby aged from 1 to 12 months - 80 to 140
Baby/toddler aged from 1 to 2 years - 80 to 130
Toddler/young child aged 2 to 6 years - 75 to 120
Child aged 7 to 12 years - 75 to 110
Adult aged 18+ years - 60 to 100
Adult athlete - 40 to 60
(There is a considerable amount of overlap from 14 to 17 years of age, with younger and older ages, depending on which health authorities you use for data)

Checking your own heart rate:
The wrist (the radial artery) - place the palm of your hand facing upward. Place two fingers on the thumb side of your wrist gently, you will sense your pulse beating there. Either count them for up to one minute, or thirty seconds and then multiply by two. Counting for 15 seconds and then multiplying by four is less accurate. It is also possible to test the pulse by touching the other side of the wrist, where the ulnar artery is.
The neck (the carotid artery) - place the index and third fingers on the neck, next to your windpipe. When you feel your pulse, either count for the whole sixty seconds, or do it in a 30 or 15 second spell and multiply by two or four.
The human heart rate may also be measured at the following points:

The brachial artery - under the biceps or inside the elbow
Abdominal aorta - over the abdomen
Apex of the heart - by placing your hand or fingers on the chest
Basilar artery - at the side of the head, close to the ear
Dorsalis pedis - the middle of dorsum of the foot
Superficial temporal artery - the temple
The facial artery - the lateral edge of the mandible
The femoral artery - in the groin
The posterior tibial artery - behind the medial malleoulus of the feet


Testing the pulse rate at the radial artery


An electrocardiograph, also known as an ECG or EKG is a more accurate way of checking a patient's heartbeat. ECGs are commonly used in critical care medicine, and many other fields of medicine.

Sports shops sell heart-rate watches that communicate with a device you strap around your chest. The readings on your watch tell you what your heart rate is - some can even work out heart-rate averages over set periods, such as the whole of an exercise session.

Bear in mind that your heart rate can be influenced by several factors, such as:
Your level of physical activity at the time
How fit you are
The ambient temperature
The position of your body - standing, sitting, lying down, etc.
Your mental and/or emotional state - excitement, anger, fear, anxiety, and other factors can raise your heart beat
The size of your body
Some medications
Bradycardia - a medical term that refers to a heart beat that is too slow, such as below 60 beats per minute (for a non-athlete)

Tachycardia - a medical term that refers to a resting heart beat of more than 100 beats per minute, an excessively fast heart beat for an adult

If you think you have bradycardia or tachycardia, see your doctor, especially if you are also short of breath, feel dizzy, and/or have fainting episodes.
What is your maximum heart rate?
This is the maximum number of times your heart can beat per minute. It is a useful measure for sports people, so they can gauge their training intensities.

There are two ways you can find out what your maximum heart rate is:
Have it clinically tested - usually by a cardiologist or an exercise physiologist. People over 35 years of age who are overweight or have not done exercise for a long time are advised to have their maximum heart rates clinically tested by a trained health care professional. The health care professional may use a treadmill and a electrocardiograph.
Predicted maximum heart rate - this involves using a mathematical formula, called the age-adjusted formula.

For adult males: 220 minus your age. For a 25 year-old man it would be 195 bpm (220 minus 25)

For adult females: 226 minus your age. For a 25 year-old woman it would be 201 bpm (226 minus 25)

It is important to remember that this formula gives a rough figure, a ballpark figure. Ideally, you should have your maximum heart beat measured clinically.

Is A Mole Benign Or Cancerous? New Staining Test Can Provide New Measure

Up till now, finding out if a mole is a potentially life-threatening melanoma has been a complex task, resulting in both under- and over diagnosis. However, a novel diagnostic staining test has been designed, developed and studied by investigators at Weill Medical College. According to the researchers, the test can provide a new measure of determining whether a mole is benign or cancerous, and has the potential for expanded use across all cancers. The study is published in the Nov. 21 issue of the Archives of Dermatology.

The researchers explain that the novel test, which relies on the soluble adenylyl cyclase (sAC) expression pattern, provides objective results - melanoma is present if sAC is present in the nucleus of cells from a skin biopsy, and benign if the nucleus is not positive.

The majority of diagnostic stains currently used highlight a particular cell in the biopsy. If the stain is more intense it tends to be melanoma, but the definition of 'intense' is subjective.


There are various types of moles, this one is a intradermal nevus

Senior author Dr. Jonathan Zippin, explains:

"The sAC stain is either positive or negative in the cell's nucleus. Other stains require an interpretation of staining intensity, which means that a diagnosis of melanoma can rest on a pathologist's opinion.

As a clinical dermatologist, this uncertainty is difficult to deal with. No one wants to miss a true diagnosis of melanoma, but telling someone they have melanoma, when they may not, changes his or her life."


In order to diagnose melanoma, the skin lesion, together with an area of healthy tissue around it, must be surgically removed, which can result in disfiguration. According to Dr. Zippin, those who are diagnosed with melanoma are concerned they might develop other forms of cancer, as individuals' diagnoses with the disease have a greater risk of developing another cancer.

sAC stain should be used together with other diagnostic tests, such as light microscopy and three other strains currently available, according to the investigation's lead author, Dr. Cynthia Margo.

Dr. Zippin, said:

"What I hope is that five years down the line, this and other stains will help pathologists remove any uncertainty as to whether a biospy is worrisome."


Dr. Margo explains, however, that the sAC provides one benefit that other stains do not. "The greatest practical application of sAC is using it to determine the cancer-free margins of a lentigo maligna that needs to be removed. This is a common melanoma in situ, usually found on the face, that does not show invasive growth. But until the development of sAC, it was very difficult to tell where the cancerous lesion ended." The sAC stain, which Margo uses on several patients, "is vastly superior to any other test we have now to determine margins."

Dr. Zippin explains:

"The new stain is a monoclonal antibody that binds to sAC, which is a signaling molecule," who has studied the molecule. He continues: "sAC senses changes in the interior of cells, such as pH and metabolism, and responds by regulating gene expression, metabolism and growth."


The sAC protein was discovered by Dr. Jochen Buck and Dr. Lonny Levin, both professors of pharmacology at Weill Cornell Medical College.

Dr. Zippin and Dr. Margo developed the antibody used to develop the diagnostic test. As their research gained potential, Dr. Zippin, Dr. Margo, Dr. Buck and Dr. Levin created a company called Cutting Edge Pattern Biotech in order to share the antibody with the scientific community. At present, they are scientific advisers but have no fiscal role in the company.

Dr. Zippin said:

"Beause the sAC protein is expressed in all tissues of the body, and appears to be linked to processes important for the development of cancer, we predict that immunostain will be useful for the diagnosis of many other cancers and diseases."


Even though the diagnostic stain does not require approval from the FDA, the investigators explain that Cutting Edge Pattern Biotech plans to seek federal approval of the sAC antibody as a diagnostic test.

Key To Melanoma Metastasis

Researchers from UNC Lineberger Comprehensive Cancer Center are part of a team that has identified a protein, called P-Rex1, that is key to the movement of cells called melanoblasts. When these cells experience uncontrolled growth, melanoma develops.

Melanoma is one of the only forms of cancer that is still on the rise and is one of the most common forms of cancer in young adults. The incidence of melanoma in women under age 30 has increased more than 50 percent since 1980. Metastases are the major cause of death from melanoma.

The team found that mice lacking the P-Rex1 protein are resistant to melanoma metastases. When researchers tested human melanoma cells and tumor tissue for the protein, P-Rex1 was elevated in the majority of cases - a clue that the protein plays an important role in the cancer's spread. Their findings were published in the journal Nature Communications.

"We know that mutations in a gene called BRAF are important for the development of melanoma and several years ago we published a collaborative paper listing 82 proteins that seem to be affected by this genetic pathway. From that list, we focused on P-Rex1 in collaboration with Dr. Nancy Thomas here at UNC and researchers in the United Kingdom," says Channing Der, PhD, a member of the UNC research team. Der is Kenan Professor of pharmacology at UNC-Chapel Hill and member of UNC Lineberger.

A drug approved this summer, vemurafenib, is the first treatment directed at the BRAF mutation. Clinical trials found that the treatment offers a significant survival benefit.

"We think that vemurafenib may work, in part, by blocking the up-regulation of P-Rex1," Der adds.

"As a physician and scientist, I know firsthand the frustration of having very limited therapeutic options to offer to patients with metastatic melanoma," says Nancy Thomas, MD, PhD, whose laboratory analyzed the protein's expression in human cells. "Pinpointing that P-Rex1 plays a key role in metastasis gives us a better understanding of how vemurafenib may work and a target for developing new treatments," she adds.

Metastatic Breast And Ovarian Cancer Vaccine - Promising Results

A trial published in Clinical Cancer Research demonstrated a positive response in both metastatic breast cancer and ovarian cancer to a recombinant poxviral vaccine.

Lead investigator James Gulley, M.D., Ph.D., director and deputy chief of the clinical trials group at the Laboratory of Tumor Immunology and Biology at the National Cancer Institute commented:

"With this vaccine, we can clearly generate immune responses that lead to clinical responses in some patients."


For the trial, funded by the National Cancer Institute, Gulley and his team involved 26 patients, all of them heavily pretreated, with 21 patients receiving at least three prior chemotherapy treatments, and designated them to receive monthly vaccinations with PANVAC vaccine that contains transgenes for MUC-1, CEA and three T cell costimulatory molecules.

In 12 breast cancer patients the team established an average time to disease progression of 2.5 months and an average overall survival rate of 13.7 months. In four patients the disease was stable. The average time to progression for the 14 ovarian cancer patients was two months and the average survival rate of 15 months.

The most common side effect after treatment was mild reactions at the injection-site.

Because of the rising interest in cancer vaccinations, Gulley recommends for further studies to be conducted in order to establish which vaccines are beneficial for particular patients.

He concludes:

"The sustained benefit seen in some patients in this study underscores the potential for therapeutic vaccines to impact clinical outcomes without toxicity. However, more studies in the appropriate patient populations are required to adequately assess efficacy."

Wi-Fi Laptops Harm Sperm Motility And Increase Sperm DNA Fragmentation

Males who place a laptop on their laps with the WI-FI on might have a greater risk of reduced sperm motility and more sperm DNA fragmentation, which could, in theory, undermine their chances of becoming fathers, researchers from Nascentis Medicina Reproductiva, Argentina, and the Eastern Virginia Medical School, USA, reported in the journal Fertility and Sterility this week. Sperm motility refers to the percentage of sperm in a semen sample that are moving - normally, a high percentage of all sperm should be moving (thrashing their tails and swimming).

This study was done in an artificial setting. The male participants were not tested with the laptops on their laps - semen samples were taken, placed under laptops for four hours, and then analyzed.

Previous studies had already shown that placing a laptop on a man's lap could potentially affect his fertility, especially if this occurs frequently and for long periods. The laptop can cause scrotal hyperthermia (elevated testicle temperature), which can considerably affect the quality of his sperm (Link to 2010 study).

In this new study, the authors explain that not only might the laptop-on-lap undermine semen quality, but also the Wi-Fi, if the laptop is near semen. They found that there was less damage when there was no Wi-Fi signal than when there was.

The double-whammy of the Wi-Fi signal and laptop temperature can cause:
A decrease in human sperm motility
Sperm DNA fragmentation - irreversible changes in the genetic code
Perhaps the electromagnetic radiation emitted by Wi-Fi damages the semen, the scientists suggested.

Wi-Fi stands for "wireless fidelity". The term refers to a group of technical standards which enable the transmission of data over wireless networks. Put simply: Wi-Fi means wireless internet connection.

Conrado Avendaño and team carried out a study involving semen samples from 29 healthy and fertile males. They experimented on their semen samples in two environments:
The Wi-Fi sample. A few drops of semen were place under a laptop with the Wi-Fi switched on. The laptop was downloading data from the internet non-stop.
The non-Wi-Fi sample. Identical to the environment above, but with no Wi-Fi switched on.
Four hours later, they found:
One quarter of the sperm had lost motility in the Wi-Fi samples
14% of the sperm had lost motility in the non-Wi-Fi samples
9% of the sperm showed DNA damage in the Wi-Fi samples
3% of the sperm showed DNA damage in the non-Wi-Fi sampes
Avendaño said:

"Our data suggest that the use of a laptop computer wirelessly connected to the internet and positioned near the male reproductive organs may decrease human sperm quality.
,br> At present we do not know whether this effect is induced by all laptop computers connected by Wi-Fi to the internet or what use conditions heighten this effect."


The authors carried out a separate test to determine what the EM radiation levels might be near a Wi-Fi connected laptop and a non-Wi-Fi one. The difference was significant - when the computer was not Wi-Fi connected EM radiation readings were "negligible".

According to PC Mag, Electromagnetic Radiation, also known as EM Radiation, or EMR is:

"The energy that radiates from all things in nature and from man-made electronic systems. It includes cosmic rays, gamma rays, x-rays, ultraviolet light, visible light, infrared light, radar, microwaves, TV, radio, cellphones and all electronic transmission systems. Electromagnetic radiation is made up of electric and magnetic fields that move at right angles to each other at the speed of light."


The authors, as well as other experts who have commented on this study, stress that until a long-term study with a larger group of men and in natural environments is carried out, this one is only "interesting" and not really biologically relevant for humans.

Even though previous studies have looked at laptop usage and sperm quality, none have determined whether there is any impact on how many children men subsequently have or don't have.

In an Abstract in the journal, the authors concluded:

"To our knowledge, this is the first study to evaluate the direct impact of laptop use on human spermatozoa. Ex vivo exposure of human spermatozoa to a wireless internet-connected laptop decreased motility and induced DNA fragmentation by a nonthermal effect.

We speculate that keeping a laptop connected wirelessly to the internet on the lap near the testes may result in decreased male fertility. Further in vitro and in vivo studies are needed to prove this contention."

Coffee Emerges As Protective Against Cancer And Other Diseases

Starbucks fans around the world can rejoice that their tipple gets the thumbs up yet again. Already shown to protect against a number of diseases, a recent study in the Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, shows coffee drinkers who consume more than four cups a day have a 25% lower risk of developing Endometrial Cancer. It is thought that the antioxidant properties in coffee may be a part of the mechanism.

Edward Giovannucci, M.D., Sc.D., professor of nutrition and epidemiology at the Harvard School of Public Health, and a senior researcher on the study, said coffee is starting to be proven as a protective agent in cancers that are linked to obesity, estrogen and insulin.

He said :

"Coffee has already been shown to be protective against diabetes due to its effect on insulin ... So we hypothesized that we'd see a reduction in some cancers as well."


Giovannucci, and his colleagues, including Youjin Je, a doctoral candidate in his lab, looked at endometrial cancer cases in nearly 70,000 women who enrolled in the Nurse's Health Study. Over 26 years they documented 672 cases of endometrial cancer. More than four cups of coffee was linked with a 25% decrease in risk, while two to three cups had a 7% lower risk.

The results seemed to hold true for decaf as well, with a 22% reduction for more than two cups per day.

Giovannucci said he'd like to see further research on the effects of coffee on cancer, because in this and similar studies, coffee intake is self-selected and not randomized.

He said :

"Coffee has long been linked with smoking, and if you drink coffee and smoke, the positive effects of coffee are going to be more than outweighed by the negative effects of smoking ... However, laboratory testing has found that coffee has much more antioxidants than most vegetables and fruits."

Atherosclerosis Pathology

Definition

The term atherosclerosis is derived from the Greek "athero," meaning gruel, or wax, corresponding to the necrotic core area at the base of the atherosclerotic plaque, and "sclerosis" for hardening, or induration, referring to the fibrous cap of the plaque's luminal edge.

The earliest pathologic descriptions of atherosclerotic lesions focused on morphologies of fatty streaks to fibroatheromas (FAs) and advanced plaques complicated by hemorrhage, calcification, ulceration, and thrombosis. In the mid 1990s the terminology used to define atheromatous plaques was refined by the American Heart Association (AHA) Consensus Group headed by Dr. Stary.{{Ref2}

The classification consists of 6 different numeric categories to include early lesions of initial type I, adaptive intimal thickening; type II, fatty streak; and type III, transitional or intermediate lesions; and advanced plaques characterized as type IV, atheroma; type V, fibroatheroma or atheroma with thick fibrous cap; and type VI, complicated plaques with surface defects, and/or hematoma-hemorrhage, and/or thrombosis.

A modified version of the AHA classification was developed by our laboratory to include important pathologic lesions responsible for luminal thrombosis other than plaque rupture, such as plaque erosion and calcified nodule.[1] In this modified classification, numeric AHA lesions types I to IV are replaced by descriptive terminology to include adaptive intimal thickening, intimal xanthoma, pathologic intimal thickening (PIT), and fibroatheroma, as shown in the table below.

Lesion reference to AHA types V and VI was discarded, because it failed to account for the 3 different morphologies (rupture, erosion, and calcified nodule) that give rise to acute coronary thrombosis.

Epidemiology

Coronary artery disease remains the leading cause of death in the Western world. A new or recurrent myocardial infarction afflicts approximately 1.1 million people in the USA per year, of which 40% are fatal. Sudden cardiac death as a first manifestation of the atherosclerotic process occurs in >450,000 individuals annually. The vast majority of acute myocardial infarctions (approximately 75%) occur from plaque rupture; other causes of coronary thrombosis include erosion and calcified nodules.[3]

Although lesions with rupture occur in men of all ages (this is consistent for all plaque morphologies with thrombi), the frequency of sudden coronary death decreases with advancing age. The incidence of rupture varies with each decade, and the highest incidence of plaque rupture is seen in the 40s in men, whereas in women the incidence increases beyond age 50 years. Approximately 80% of coronary thrombi in women older than 50 years occur from plaque rupture, and there is a strong association with circulating cholesterol. In acute myocardial infarction or sudden coronary death, plaque erosion occurs primarily in patients younger than 50 years and represents the majority of acute coronary thrombi in premenopausal women. Furthermore, 20-25% of acute myocardial infarcts occurring in hospitalized patients are due to plaque erosion.

The etiology of atherosclerosis is unknown, but there are multiple factors that contribute to atherosclerotic plaque progression. These include genetic and acquired factors. Processes involved in atherosclerosis include coagulation, inflammation, lipid metabolism, intimal injury, and smooth muscle cell proliferation (see the image below).

Factors that affect these processes may inhibit or accelerate atherosclerosis. The most common risk factors are family history, hyperlipidemia, diabetes mellitus, cigarette smoking, hypertension, and dietary deficiencies of antioxidants.[4] Early lesion development is marked by lipid retention with activation of endothelial adhesion molecules. Inflammatory macrophages play a significant role throughout all phases of atherosclerotic progression; hyperlipidemia-induced macrophage infiltration of the arterial intima is one of the earliest pathologic changes.

A major event in atherosclerotic plaque progression is thrombosis, which may occur in any arterial bed (coronary, aorta, carotid, etc.) Three different morphologies (rupture, erosion and calcified nodule) may give rise to acute coronary thrombosis. Plaque rupture is defined by fibrous cap disruption or fracture, whereby the overlying thrombus is in continuity with the underlying necrotic core. Plaque erosion is identified when serial sectioning through a thrombus fails to show communication with a necrotic core or deep intima; the endothelium is absent, and the thrombus is superimposed on a plaque substrate primarily composed of smooth muscle cells and proteoglycans. Calcified nodules are characterized by eruptive dense calcified bodies protruding into the luminal space and represent the least frequent morphology associated with luminal thrombosis. See the following diagram.
Atherosclerosis occurs in elastic and muscular arteries and may occur iatrogenically in vein grafts interposed in the arterial circulation. The aorta is affected earliest, followed by the carotid arteries, coronary arteries, and iliofemoral arteries. Initially, lesions are most common at branch points, at sites of low shear, where a predilection to plaque formation has been observed. Coronary lesions, including thrombi occuring at atherosclerotic sites, are most prevalent in the proximal coronary arteries: the proximal left anterior descending coronary artery, followed by the right and left circumflex coronary arteries.

Atherosclerosis causes symptoms by arterial obstruction, embolization of plaque material, and weakening with rupture of the arterial wall. Obstruction with or without embolization causes ischemia of the circulation supplied by the vessel. Ischemic strokes result from atherosclerosis of the carotid arteries and aortic arch, which embolize thrombi and atherosclerotic material, as well as local atherosclerosis of the cerebral vessels.

Obstruction of coronary arteries causes myocardial ischemia. Myocardial ischemia may present as acute coronary syndromes (acute ST elevation infarct, non-ST elevation infarct, and unstable angina), sudden death, or chronic congestive heart failure. Obstruction of iliac vessels results in ischemia of the lower extremities (claudication). Atherosclerotic aneurysms show a predilection for the aorta, especially the abdominal aorta. Aortic aneurysms may rupture and cause death by hemorrhage into the retroperitoneal space or pleural cavities, depending on the location.

The gold standard for imaging atherosclerotic lesions of the coronary circulation is angiography. Newer imaging modalities, such as cardiac magnetic resonance imaging (MRI), are being developed that may provide less invasive methods of determining sites of stenosis. Imaging of atherosclerotic lesions of the carotid circulation include carotid ultrasonography, a noninvasive technique.


Gross Findings

In the aorta, atherosclerotic lesions have been classified largely on gross findings. Fatty streaks are yellow, minimally raised lesions that demonstrate abundant lipid when stained with oil red O. Fibrous plaques are raised, white, firmer areas that are relatively well demarcated. Ulcerated plaques demonstrate surface thrombosis and represent ruptured fibroatheromas.

Coronary lesions, when cut on cross-section, show bright yellow cores when there is abundant extracellular lipid, as in fibroatheromas. Ruptured or eroded plaques demonstrate a luminal thrombus, which is pale red or tan in the unfixed state, depending on the proportion of fibrin, platelets, and entrapped red blood cells. Calcified plaques are hard and brittle, are difficult to cute with a scalpel blade, and must be decalcified during or after fixation so that sections for microscopy may be performed.

The gross findings of carotid plaques are similar to those of the coronary arteries. There is often calcification, which can be seen and felt as mineral deposits. Atheromas are bright yellow on cross-section, and atheromas with intraplaque hemorrhage show a more variegated yellow-red cut surface. Fibrous plaques are homogeneous, firm and white, and often show areas of calcification.