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Mango fruit been found to prevent or stop certain colon and breast cancer cells in the lab.
That's according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden.
Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value.
"If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there," said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. "In comparison with antioxidants in blueberry, acai and pomegranate, it's not even close."
But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted.
"It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food," she said. "It would be good to include mangoes as part of the regular diet."
The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health.
Mango showed some impact on lung, leukemia and prostate cancers but was most effective on the most common breast and colon cancers.
"What we found is that not all cell lines are sensitive to the same extent to an anticancer agent," she said. "But the breast and colon cancer lines underwent apotosis, or programmed cell death. Additionally, we found that when we tested normal colon cells side by side with the colon cancer cells, that the mango polyphenolics did not harm the normal cells."
The duo did further tests on the colon cancer lines because a mango contains both small molecules that are readily absorbed and larger molecules that would not be absorbed and thus remain present in a colon.
"We found the normal cells weren't killed, so mango is not expected to be damaging in the body," she said. "That is a general observation for any natural agent, that they target cancer cells and leave the healthy cells alone, in reasonable concentrations at least."
The Talcotts evaluated polyphenolics, and more specifically gallotannins as being the class of bioactive compounds (responsible for preventing or stopping cancer cells). Tannins are polyphenols that are often bitter or drying and found in such common foods as grape seed, wine and tea.
The study found that the cell cycle, which is the division cells go through, was interrupted. This is crucial information, Suzanne Talcott said, because it indicates a possible mechanism for how the cancer cells are prevented or stopped.
"For cells that may be on the verge of mutating or being damaged, mango polyphenolics prevent this kind of damage," she said.
The Talcotts hope to do a small clinical trial with individuals who have increased inflamation in their intestines with a higher risk for cancer.
"From there, if there is any proven efficacy, then we would do a larger trial to see if there is any clinical relevance," she said.
According to the National Mango Board, based in Winter Park, Fla., most mangoes consumed in the U.S. are produced in Mexico, Ecuador, Peru, Brazil, Guatemala and Haiti. Mangoes are native to southeast Asia and India and are produced in tropical climates. They were introduced to the U.S. in the late 1800s, and a few commercial acres still exist in California and Florida.
Determining the type of seizure that has occurred is essential for focusing the diagnostic approach on particular etiologies, selecting the appropriate therapy, and providing potentially vital information regarding prognosis. In 1981, the International League Against Epilepsy (ILAE) published a modified version of the International Classification of Epileptic Seizures that has continued to be a useful classification system (Table 348-1). This system is based on the clinical features of seizures and associated electroencephalographic findings. Other potentiallydistinctive features such as etiologyor cellular substrate are not considered in this classification system, although this will undoubtedlychange in the future as more is learned about the pathophysiologic mechanisms that underlie specific seizure types.
A fundamental principle is that seizures maybe either partial (synonymous with focal) or generalized. Partial seizures are those in which the seizure activityis restricted to discrete areas of the cerebral cortex.
Generalized seizures involve diffuse regions of the brain simultaneously. Partial seizures are usually associated with structural abnormalities of the brain. In contrast, generalized seizures mayresult from cellular, biochemical, or structural abnormalities that have a more widespread distribution.
PARTIAL SEIZURES
Partial seizures occur within discrete regions of the brain. If consciousness is fullypreserved during the seizure, the clinical manifestations are considered relativelysimple and the seizure is termed a simple partial seizure. If consciousness is impaired, the symptomatology is more complex and the seizure is termed a complex partial seizure. An important additional subgroup comprises those seizures that begin as partial seizures and then spread diffuselythroughout the cortex, i.e., partial seizures with secondary generalization.
Simple Partial Seizures Simple partial seizures cause motor, sensory,autonomic, or psychic symptoms without an obvious alteration in consciousness. For example, a patient having a partial motor seizure arising from the right primarymotor cortex in the vicinitycontrolling hand movement will note the onset of involuntarymovements of the contralateral, left hand. These movements are typically clonic (i.e., repetitive,flexion/extension movements) at a frequencyof 2 to 3 Hz; pure tonic posturing maybe seen as well. Since the cortical region controlling hand movement is immediatelyadjacent to the region for facial expression, the seizure mayalso cause abnormal movements of the face synchronous with the movements of the hand. The electroencephalogram (EEG) recorded with scalp electrodes during the seizure (i.e., an ictal EEG) mayshow abnormal discharges in a verylimited region over
the appropriate area of cerebral cortex if the seizure focus involves the cerebral convexity. Seizure activity occurring within deeper brain structures is often not recorded bythe standard EEG, however, and mayrequire intracranial electrodes for its detection.
Three additional features of partial motor seizures are worth noting.First, in some patients the abnormal motor movements maybegin in a veryrestricted region such as the fingers and graduallyprogress (over seconds to minutes) to include a larger portion of the extremity. This phenomenon, described byHughlings Jackson and known as a “Jacksonian march,” represents the spread of seizure activityover a progressivelylarger region of motor cortex. Second, patients mayexperience a
localized paresis (Todd’s paralysis) for minutes to many hours in the involved region following the seizure. Third, in rare instances the seizure maycontinue for hours or days. This condition, termed epilepsia partialis continua, is often refractoryto medical therapy.
Simple partial seizures mayalso manifest as changes in somaticsensation (e.g., paresthesias), vision (flashing lights or formed hallucinations), equilibrium (sensation of falling or vertigo), or autonomic function (flushing, sweating, piloerection). Simple partial seizures arising from the temporal or frontal cortex mayalso cause alterations in hearing, olfaction, or higher cortical function (psychic symptoms).
This includes the sensation of unusual, intense odors (e.g., burningrubber or kerosene) or sounds (crude or highlycomplex sounds), or an epigastric sensation that arises from the stomach or chest to the head.Some patients describe odd, internal feelings such as fear, a sense ofimpending change, detachment, depersonalization, deja ` vu, or illusions that objects are growing smaller (micropsia) or larger (macropsia). When such symptoms precede a complex partial or secondarily gen-
eralized seizure, these simple partial seizures serve as a warning, or aura.
Complex Partial Seizures Complex partial seizures are characterized by focal seizure activityaccompanied bya transient impairment of the
patient’s abilityto maintain normal contact with the environment. The patient is unable to respond appropriatelyto visual or verbal commands during the seizure and has impaired recollection or awareness of the ictal phase. The seizures frequentlybegin with an aura (i.e., a simple partial seizure) that is stereotypic for the patient. The start of the ictal phase is often a sudden behavioral arrest or motionless stare, which marks the onset of the period of amnesia. The behavioral arrest is usuallyaccompanied by automatisms, which are involuntary, automatic behaviors that have a wide range of manifestations. Automatisms mayconsist of verybasic behaviors such as chewing, lip smacking, swallowing, or “picking” movements of the hands, or more elaborate behaviors such as a displayof emotion or running. The patient is typically confused following the seizure, and the transition to full recoveryof consciousness mayrange from seconds up to an hour.
Examination immediatelyfollowing the seizure mayshow an anterograde amnesia or, in cases involving the dominant hemisphere, a postictal aphasia.
The routine, interictal (i.e., between seizures) EEG in patients with complex partial seizures is often normal or mayshow brief discharges termed epileptiform spikes,or sharp waves. Since complex partial seizures can arise from the medial temporal lobe or inferior frontal lobe,i.e., regions distant from the scalp, the EEG recorded during the seizure maybe nonlocalizing. However, the seizure focus is often detected using sphenoidal or surgicallyplaced intracranial electrodes.
The range of potential clinical behaviors linked to complex partial seizures is so broad that extreme caution is advised before concluding that stereotypic episodes of bizarre or atypical behavior are not due to seizure activity. In such cases additional, detailed EEG studies may be helpful.
Partial Seizures with Secondary Generalization Partial seizures can spread to involve both cerebral hemispheres and produce a generalized seizure, usuallyof the tonic-clonic variety(discussed below). Secondary generalization is observed frequentlyfollowing simple partial seizures, especiallythose with a focus in the frontal lobe, but mayalso be associated with partial seizures occurring elsewhere n the brain. A partial seizure with secondarygeneralization is often difficult to distin-
guish from a primarilygeneralized tonic-clonic seizure, since bystanders tend to emphasize the more dramatic, generalized convulsive phase of the seizure and overlook the more subtle, focal symptoms present at onset. In some cases, the focal onset of the seizure becomes apparent onlywhen a careful historyidentifies a preceding aura (i.e., simple partial seizure). Often, however, the focal onset is not clinically evident and maybe established onlythrough careful EEG analysis.
Nonetheless, distinguishing between these two entities is extremely important, as there maybe substantial differences in the evaluation and treatment of partial versus generalized seizure disorders.
GENERALIZED SEIZURES
Bydefinition, generalized seizures arise from both cerebral hemispheres simultaneously. However, it is currently impossible to exclude entirelythe existence of a focal region of abnormal activitythat initiates the seizure prior to rapid secondarygeneralization. For this reason, generalized seizures maybe practically defined as bilateral clinical and electrographic events without any detectable focal onset. Fortunately, several types of generalized seizures have distinctive features that facilitate clinical diagnosis.Absence Seizures (Petit Mal) Absence seizures are characterized bysudden, brief lapses of consciousness without loss of postural control. The seizure typically lasts for only seconds, consciousness returns as suddenlyas it was lost, and there is no postictal confusion. Although the brief loss of consciousness maybe clinicallyinapparent or the sole manifestation of the seizure discharge, absence seizures are usually accompanied bysubtle, bilateral motor signs such as rapid blinking of the eyelids, chewing movements, or small-amplitude, clonic movements of the hands.
Absence seizures usuallybegin in childhood (ages 4 to 8) or early adolescence and are the main seizure type in 15 to 20% of children with epilepsy. The seizures can occur hundreds of times per day, but the child maybe unaware of or unable to conveytheir existence. The patient maybe constantlypiecing together experiences that have been interrupted bythe seizures. Since the clinical signs of the seizures are subtle, especiallyto new parents, it is not surprising that the first clue to absence epilepsyis often unexplained “daydreaming” and a decline
in school performance recognized bya teacher. The electrophysiologic hallmark of typical absence seizures is a generalized, symmetric, 3-Hz spike-and-wave discharge that begins and ends suddenly, superimposed on a normal EEG background. Pe-
riods of spike-and-wave discharges lasting more than a few seconds usuallycorrelate with clinical signs, but the EEG often shows many more brief bursts of abnormal cortical activitythan were suspected clinically. Hyperventilation tends to provoke these electrographic discharges and even the seizures themselves and is routinelyused when recording the EEG.
Typical absence seizures are often associated with generalized, tonic-clonic seizures, but patients usuallyhave no other neurologic
problems and respond well to treatment with specific anticonvulsants.Although estimates vary, 60 to 70% of such patients will have a spontaneous remission during adolescence.
A seizure (from the Latin sacire, “to take possession of”) is a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of central nervous system (CNS) neurons. Depending on the distribution of discharges, this abnormal CNS activitycan have various manifestations, ranging from dramatic convulsive activityto experiential phenomena not readilydiscernible byan observer.Although a varietyof factors influence the incidence and prevalence of seizures, 5 to 10% of the population will have at least one seizure,
with the highest incidence occurring in earlychildhood and late adult-hood.
The meaning of the term seizure needs to be carefullydistinguished from that of epilepsy. epilepsy describes a condition in which a person has recurrent seizures due to a chronic, underlying process. This definition implies that a person with a single seizure, or recurrent seizures due to correctable or avoidable circumstances, does not necessarily have epilepsy. Epilepsy refers to a clinical phenomenon rather than a
single disease entity, since there are many forms and causes of epilepsy. However, among the many causes of epilepsy there are various epilepsy syndromes in which the clinical and pathologic characteristics are distinctive and suggest a specific underlying etiology.
Using the definition of epilepsyas two or more unprovoked seizures, the incidence of epilepsyis 0.3 to 0.5% in different populations throughout the world, and the prevalence of epilepsyhas beenestimated at 5 to 10 persons per 1000.
Studying animals in behavioral experiments has been a cornerstone of psychological research, but whether the observations are relevant for human behavior has been unclear. Weill Cornell Medical College researchers have identified an alteration to the DNA of a gene that imparts similar anxiety-related behavior in both humans and mice, demonstrating that laboratory animals can be accurately used to study these human behaviors.
The findings may help researchers develop new clinical strategies to treat humans with anxiety disorders, such as phobias and post-traumatic stress disorder (PTSD).
Results from the study, funded by the National Institutes of Health, are published January 15 in the journal Science.
"We found that humans and mice who had the same human genetic alteration also had greater difficulty in extinguishing an anxious-like response to adverse stimuli," explains Dr. B.J. Casey, co-senior author of the study and professor of psychology in psychiatry from The Sackler Institute for Developmental Psychobiology at Weill Cornell Medical College.
The researchers observed common behavioral responses between humans and mice that possess an alteration in the brain-derived neurotrophic factor (BDNF) gene. The mice were genetically altered -- meaning that they had a human genetic variation inserted within their genome.
To make their comparison, the researchers paired a harmless stimulus with an aversive one, which elicits an anxious-like response, known as conditioned fear. Following fear learning, exposure to numerous presentations of the harmless stimulus alone, in the absence of the aversive stimulus, normally leads to subjects extinguishing this fear response. That is, a subject should eventually stop having an anxious response towards the harmless stimulus.
"But both the mice and humans found to have the alternation in the BDNF gene took significantly longer to 'get over' the innocuous stimuli and stop having a conditioned fear response," explains Dr. Fatima Soliman, lead author of the study, who is currently a Tri-Institutional MD-PhD student, and has completed her Ph.D. in the labs of Drs. B.J. Casey and Francis S. Lee.
In addition to the observational testing, the researchers also performed brain scans using functional magnetic resonance imaging (fMRI), on the human participants, to see if brain function differed between people with the abnormal BDNF gene and those with normal BDNF genes.
They found that a circuit in the brain involving the frontal cortex and amygdala -- responsible for learning about cues that signal safety and danger -- was altered in people with the abnormality, when compared with control participants who did not have the abnormality.
"Testing for this gene may one day help doctors make more informed decisions for treatment of anxiety disorders," explains Dr. Francis S. Lee, co-senior author of the study and associate professor of psychiatry and pharmacology at Weill Cornell Medical College.
Therapists use exposure therapy -- a type of behavior therapy in which the patient confronts a feared situation, object, thought, or memory -- to treat individuals who experience stress and anxiety due to certain situations. Sometimes, exposure therapy involves reliving a traumatic experience in a controlled, therapeutic environment and is based on principles of extinction learning. The goal is to reduce the distress, physical or emotional, felt in situations that trigger negative emotion. Exposure therapy is often used for the treatment of anxiety, phobias and PTSD.
"Exposure therapy may still work for patients with this gene abnormality, but a positive test for the BDNF genetic variant may let doctors know that exposure therapy may take longer, and that the use of newer drugs may be necessary to accelerate extinction learning," explains Dr. Soliman.
Co-authors of the study include Dr. Charles Glatt, Dr. Kevin Bath, Dr. Liat Levita, Rebecca Jones, Siobhan Pattwell, Dr. Deqiang Jing, Dr. Nim Tottenham, Dr. Dima Amso, Dr. Leah Somerville, Dr. Henning Voss, Dr. Douglas Ballon, Dr. Conor Liston, Theresa Teslovich and Tracey Van Kempen, all from Weill Cornell; and Dr. Gary Glover, from Stanford University, Stanford, Calif.
The discovery of an inflammatory mediator key to the blinding effects of diabetic retinopathy is pointing toward a potential new treatment, Medical College of Georgia researchers said.
Interleukin-6, known to contribute to the debilitating joint inflammation of rheumatoid arthritis, also helps ignite inflammation of the retina, a first step in a disease that is the leading cause of blindness is working-age adults, MCG researchers reported online in Investigative Ophthalmology & Visual Science.
The finding has the scientists looking at whether an interleukin-6 antibody, which is showing success in treating rheumatoid arthritis, can halt inflammation in mice with diabetic retinopathy. "We expect that this neutralizing antibody can be used to treat diabetic retinopathy in the future," said Dr. Wenbo Zhang, assistant research scientist in MCG's Vascular Biology Center. Drs. Zhang and Modesto Rojas, senior postdoctoral fellow, are co-first authors on the paper.
Angiotensin II, a powerful constrictor of blood vessels, is typically associated with the kidneys where it plays a vital role in regulating blood pressure. The scientists suspect angiotensin II helps promotes wound healing and regulation of pressure within small blood vessels in the eye.
However in diabetes, angiotensin II levels increase in the eye -- probably in response to high glucose levels -- and help promote inflammation, spurring remodeling of blood vessels and tissue destruction, Dr. Rojas said. "Vascular inflammation is one of the first steps to inducing the changes in the retina."
MCG scientists have shown interleukin-6 is a needed accomplice whose previously undetectable levels in the eye also increase, said Dr. Ruth Caldwell, cell biologist a the Vascular Biology Center and the Charlie Norwood Veterans Affairs Medical Center and the study's corresponding author.
With the help of interleukin-6, angiotensin II induces white blood cells to stick to the endothelial cells lining blood vessels of the retina, which slows blood flow. The white blood cells also start producing inflammatory and vascular growth factors that cause blood vessel walls to leak and thicken, further constricting blood flow. Retinal cells start dying from the reduced blood and oxygen supplies that result. In response, the body prompts growth of new blood vessels, presumably to help but instead causing more vision impairment.
If the trigger, high glucose, was temporary, these natural responses might help clear damaged cells and protect the eye. "Inflammation is a compensatory mechanism that gets activated as a survival mechanism," Dr. Rojas said. "If it continues, the effect is bad."
"We have known for along time if patients keep their blood sugar under perfect control, they don't have these problems, but that's hard," Dr. Caldwell adds. "That is why it's such a difficult disease."
To examine interleukin-6's role in the destruction, the researchers injected angiotensin II into the vitreous portion of the eyes of mice missing the gene for the inflammatory factor as well as normal mice. The extra angiotensin did little to the retinal vessels of mice lacking interleukin-6 but vessels in the normal mouse retina mimicked the inflammatory reaction found in diabetic retinopathy. When they reintroduced interleukin-6 to the genetically altered mice, the damage mimicked that of the normal mice. "So when we knock out interleukin-6, we can block the effects of angiotensin II," Dr. Caldwell said.
The scientists want to see whether the interleukin-6 antibody can be used to prevent damage by giving it shortly after the onset of diabetes in rodents and as a treatment by using it later in the disease process.
The research was funded by the National Institutes of Health, the Department of Veterans Affairs and postdoctoral fellowship awards from the Juvenile Diabetes Research Foundation International and the American Heart Association.
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Frequent testing and treatment of infection does not reduce the prevalence of chlamydia in urban teenage girls, according to a long-term study by Indiana University School of Medicine researchers published in the January 1, 2010 issue of the Journal of Infectious Diseases.
Despite the fact they were screened every three months and treated when infected, the proportion of infected girls did not change over the course of the study. On entering the study, 10.9 percent of the young women were infected. After 18 months of participation, 10.6 percent were infected; 10.4 percent were infected at the four-year mark.
Eighty-four percent of repeated infections were reinfections. In spite of being so highly motivated that they kept diaries of their sexual encounters and interacted at least quarterly with the study staff, some of the young women had unprotected sex with either an untreated partner or a new partner and subsequent infection occurred. The researchers determined that 13 percent of repeated infections were due to failure of antibiotics to cure an earlier infection; considering all infections, antibiotic treatment was 92.1 percent effective.
"The rate of infection we found in the 365 Indianapolis girls we followed is similar to the rates reported by other researchers for girls in Denver and Baltimore, so it is likely that our important new findings on reinfection can be generalized to urban teenage girls in other cities," said Byron E. Batteiger, M.D., professor of medicine at the IU School of Medicine, an infectious disease specialist who is the first author of the study.
The researchers obtained a biological sample from as many sex partners of the study participants as possible to determine if the boys were chlamydia infected. "We were able to test 22.6 percent of all the partners that the girls named in the study. We determined that 26.2 percent of the participating boys were infected -- a very high level of infection in this pool of young men to whom young women in the study were exposed," noted Dr. Batteiger.
Current national recommendations call for routine chlamydia screening of women based on age and history of sexual activity. There is no similar recommendation for screening young men.
"The high rate of reinfection we found in our study strongly suggests there may be some real limits on what we can do to control chlamydia without doing a better job of controlling chlamydia in young men," said J. Dennis Fortenberry M.D. M.S., professor of pediatrics at the IU School of Medicine, an adolescent medicine physician who is the senior author of the study.
"We also need to make sure that sexually active teens are aware of fact that unlike some other diseases, having chlamydia and being successfully treated for it does not give the individual immunity from reoccurrence," said Dr. Fortenberry, who urges physicians to repeatedly screen adolescents for the disease.
Chlamydia is the most common bacterial sexually transmitted infection and is associated with an increased risk of pelvic inflammatory disease, ectopic pregnancy, tubal infertility, and increased susceptibility to human immunodeficiency virus infection. Chlamydia is more common in sexually active teens than in any other age group.
In addition to Dr. Batteiger and Dr. Fortenberry, co-authors of the study are IU School of Medicine faculty members Wanzhu Tu, Ph.D.; Susan Ofner, M.S.; Barbara Van Der Pol, Ph.D.; Diane R. Stothard, Ph.D.; Donald P. Orr, M.D.; and Barry P. Katz, Ph.D. In addition to their IU affiliations, Dr. Tu is a Regenstrief Institute investigator, Dr. Orr and Dr. Katz are Regenstrief Institute affiliated scientists and Dr. Van Der Pol is with the Marion County Department of Health. Dr. Stothard, formerly with the IU School of Medicine, is presently affiliated with Eli Lilly and Company. The study was funded by the National Institutes of Health.
The IU School of Medicine is located on the Indiana University-Purdue University Indianapolis campus.
ango fruit been found to prevent or stop certain colon and breast cancer cells in the lab.
Chlamydial Inclusion Bodies