Wednesday, August 14, 2013

Neuroblasts; miraculous minions which can regenerate damaged neurons.

In my previous post, about Basics of Neuroplasticity, I mentioned that most of so called normal person also have some or the other kind of mental/neurogical illness, out of them few realize it and few dont. But all that matters is how we figure out who we actually are beyond whats diagnosed or what we realize we are. Yeah its an long process, which has primary step of trusting our minds again. There are surgeries or medications that can fix the mind and also there are a lot which cant be fixed.
But neurologist or psychiatrists or let it be any "Brain Geeks", these are one crazy bunch, one cure after the other, possible or impossible, they keep on trying to succeed. Well that can be a proof that there is hope for one and all.

One such hope which exceeds everything right now in the field, and thats the embryonic cells in the brain called neuroblasts. These are produced by stem cells in the adult subventrical zone after a stroke and are zapped to the damaged tissue and make repairs. A neuroblast is a dividing cell that will develop into a neuron after undergoing a stage called cell migration phase (which is same as other normal cells by development and maintenance directed by chemical signals and mechanical signals which is activated at the end to form tissue or heal or mount an immune response).

Let me clear few basic things. Neuron, as we know is a basic unit cell of nervous system in an organism. Neural stem cell, these are committed to the neuronal fate, hence form an neuron, but these dont divide, an neural stem cell undergoes a change to form neuron which resembles an postmitotic one. Where as neuroblasts can undergoes mitosis. And another term from which your differentiate neuroblast is neuroblastoma (NB), an neuroendocrine tumor, this is extra cranial solid cancer occurring in children where ever there are nerves.

Other important fact is that the term neuroblasts was actually not segmented from Neuroepithelial cells when it was first found and described. These appear during embryonic development of the neural tube and neurogenesis. These neuroepithelial cells can differentiate into multiple types of cells, like neurons, astrocytes and other glial cells. So due to their broader generation, they are named so, but when a specific group of cells were discovered which had the capability of regenerating neurons alone, to delineate, they were named as Neuroblasts.

These neuroblasts migrate throughout the whole brain and differentiate into whats damaged. An simple example is; when injury to olfactory epithelium due to trauma, or when there is infliction of cold, leads to shedding of those smell chemo receptors, these are replaced by the migration and regeneration by neuroblasts. Other example is, there was a journal published on 29 April 2008 named Hippocampus, in this research article they write that after an hypoxic-ischemic brain injury activates early hippocampal stem/progenitor cells to replace the vulnerable neurons by the action of neuroblasts.

Well, its now possible to treat neural degeneration not just by management with medications, but direct brain to heal itself.

Tuesday, July 30, 2013

Neurological Perception and Errors of Vision

Apophenia, the "unmotivated seeing of connections" accompanied by a "specific experience of an abnormal meaningfulness", but it has come to represent the human tendency to seek patterns in random information in general (such as with gambling), paranormal phenomena, and religion.

Pareidolia is a type of apophenia involving the perception of images or sounds in random stimuli, for example, hearing a ringing phone while taking a shower, images of animals or faces in clouds, etc.

Now a few examples of the above are as follows (Respectively):

Aoccdrnig to a rscheearch at Cmabrigde Uinervtisy, it deosn’t mttaer in waht oredr the ltteers in a wrod are, the olny iprmoetnt tihng is taht the frist and lsat ltteer be at the rghit pclae. The rset can be a toatl mses and you can sitll raed it wouthit porbelm. Tihs is bcuseae the huamn mnid deos not raed ervey lteter by istlef, but the wrod as a wlohe.


What this means is that our brains rely more on context than on detail.  We derive meaning from patterns, such as language, by interrelating common characteristics and applying them to previous experience, resulting in unique interpretation of characteristics that may be historically similar, but are contextually independent.  But in the case of language, we have cause to find meaningful patterns in what may sometimes seem like complete chaos.  Language is, by definition a static pattern of visual, auditory and (most importantly) conceptual characters.

Now how is it related to Scoptoma. It’s a phenomenon when the eyes sees what the mind believes, more like the mind sees what it wants to see. So its safe to say that its not about the complex involvement of cognitive function but just the projection of an idea of our mind into our mind through the eyes.

But what is Scotoma then. Its another name for blind spot. Its the are of our retina which is posterior and medially located, from which the optic nerve arises, called as optic disk. Its named so because it lacks the receptors of light and colour. But we dont see a spot (except pathologically) in our field of vision, because the brain fills up the area in our perceptual area by arranging what could have been present. Most of the time we know what would be there without noticing, so our cortex turns it into an virtual reality.

Inattentional Blindness is an inability to perceive something that is within one's direct perceptual field because one is attending to something else. This is because perception is an limited and confined process though the stimuli are multiple at the same time. More the attention towards an particular event or events is paid, the lesser attention is towards the surrounding environment. In short, cognitive attention is towards something upon which more concentration is held. Hence this is also categorized into Cognitive Blindness.

Tuesday, July 16, 2013

Neuropsychiatry of Love

Why do we search and try being in relationships. Most of the psychiatrists say our brains are hard wired for intimate and meaning for connections with someone, hence we long for love. Reality is that it lands us in heartache and leave us either bruised or shattered. But still we try playing those odds and keep trying to get the right one. When we find the right person, yeah all the past wounds are healed, even if the relation isnt completed, even the heartfelt memory is goanna support us for rest of our lives whenever we are truly and completely alone.

So what I wanna tell now is, how is love and its effects neurologically related. Upon encountering someone that we like, they have influence over our synapse and neurotransmitters, leading to attraction, arousal, even into obsession. Now these are triggered by our continues thoughts on them, making an neurological picture of them, their thoughts, behavior. Now when we meet them in person again, our mind's map of them and their actual self vary. So question arises, do we fall in love with the person or do we love the inception of them into us which grows in our minds through time?

Following are the neurological aspects of Physiology of Love:
(These are a few aspects which as a combine, play their role in establishing this feeling)

Internal model also referred as mental model, an representation of an reality, in this case a person, in our minds. This works in this way; when we think about them all the time, we build up an internal model, an simulation which helps us predict whats gonna be their thoughts, whats their reaction towards an event or word and their feelings.

Feed forward stimulation, is a method usually used in teaching and learning where few illustrations are used for future learning and also an goal directed state of teaching, so that these are made interesting. Now best example is, to show a movie trailer to audience which could serve this purpose. Hence as a result, a person would have his own idea and structure build within his mind about that concerning thing. In fields of Behavioral and Cognitive Science, its called as "images of adaptive future behavior" or "mental time travel". In this case, it has major role in projection as love, where it prepares a mind to various outcomes, the way one has to behave and above all how to handle a particular situation during conversation. So depending on these, people judge on how charming and witty one is. Apart for that, a focus towards the goal, the ideas for that goal and the actions, hence the outcome, all these are served by this neurological process.

Error signaling and post error adaptation, this is other neurological phenomenon which is useful to maintain goal directed behavior in changing, challenging and distractive environment, where one needs to focus as well as continuously monitor ones on performance and adjust it in cases of unfavorable out comes. This is another most important process involving self assessment and surveillance of once state of mind continuously.

Temporal difference (TD) learning. This has a bit less importance, but is useful again as prediction method by sampling the environment where prediction is adjusted by supervision of observation. Example, when you are wooing a girl, its only a matter of time you will know if she would accept or reject you, so to change the outcome you depend on situations where its positive, like music, etc. which you dont plan but as per surroundings you behave or change and hence changes the outcome.
And lastly an endocrine importance in the love. Oxytocin, a mammalian neurohypophysial hormone that acts primarily as a neuromodulator in the brain which plays important role in sexual reproduction, released by the pituitary gland notably during orgasm and childbirth. It increases empathy and communication, key to sustaining a relationship between people and promotes social attraction which helps being appealing.

So as I was saying earlier, what can be love, and how would you define it as? But what if its not just their projection is what thats attractive but instead our projection about them attracts us?

Saturday, July 13, 2013

Basics of Neuroplasticity.

What is an abnormal brain? And how can it effect someone's behavior. Can it turn someone into an lame or monstrous ways. Or it would more likely manifest in some less dramatic ways. Some abnormalities are structural, showing up in scans or autopsies. But most of them are sneakier ones, mostly insidious, which are neurochemical in nature so we dont know if they are there. Few of them are treatable by surgeries, few by pills, but most of them arent actually manifesting in such that others can notice.

Now what I wanna say about is, do people really change? Is personality genetically pre programed or its shaped by oneself?

For example see how memory works in an average person, the things you see or experience remain longer if you keep reminding them. This makes the neuron circuitery active and when required its on its potential always. In the same way the everything we learn, experienced, these have greatest influence.

The science of Neuroplasticity suggests that our brain can change and grow (neuronally speaking) throughout out lives, our experiences rewire us, they can make us think or do things previously unthinkable, provoking us into forming new thoughts and ideas, teaching us valuable lessons making us less inclined into making the same mistakes of past. The brain is a constant state of flux suggesting nothing in life is permanent.

Neuroplasticity refers to changes in neural pathways and synapses which are due to changes in behavior, environment and neural processes, as well as changes resulting from bodily injury. It occurs on a variety of levels, ranging from cellular changes due to learning, to large-scale changes involved in cortical remapping in response to injury.

One of the fundamental principles of how neuroplasticity functions is linked to the concept of synaptic pruning, which is an neurological regulatory process, by reducing the overall number of neurons and synapses, leaving more efficient synaptic configurations. So individual connections within the brain are constantly being removed or recreated, largely depending upon how they are used.

Other principal involved is, if there are two nearby neurons that often produce an impulse simultaneously, their cortical maps may become one. This idea also works in the opposite way, i.e. that neurons which do not regularly produce simultaneous impulses will form different maps.
NMDA (N-methyl-D-aspartate) is the name of aselective agonist that binds to NMDA receptors, aglutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.

Long-term potentiation (LTP) is a persistent increase in synaptic strength following high-frequency stimulation of a chemical synapse. Synapses that have undergone LTP tend to have stronger electrical responses to stimuli than other synapses and lasts a very long time compared to other processes that affect synaptic strength.

Long-term potentiation (LTP), which is an increase in synaptic strength, and long- term depression (LTD), which is a decrease in synaptic strength. After only minutes of synaptic activity, there can be changes that last hours or are relatively permanent. The molecular and cellular biologies of LTP and LTD are being intensively studied, and a fascinating set of cellular processes have been discovered, which are triggered and regulated by the influx of calcium at the active synapses. It is important to recognize as well that a decrease in inhibition will facilitate changes in synaptic strength, and this links unmasking to LTP and LTD.

Understanding neuroplastic mechanisms allows us to recognize how the brain tries to repair itself. Several important principles emerge:
1. Body parts can compete for representation in the brain and use of a body part can enhance its representation. Representation areas increase or decrease depending on use. A body part is represented in various areas of the brain, both motor and sensory. The sensory representations are those that are active when sensory stimulation of that body part occurs. The motor representations are those whose activity produces movement of that body part. Representations can be determined with many techniques, including TMS and neuroimaging. A body part is not used, its representation area shrinks. For example, the representation area of the tibialis anterior is smaller after the ankle is immobilized in a cast for several weeks. In case of a stroke that damages a body part representation in the primary motor cortex, plasticity permits some reorganization that will restore a representation. This process must be competitive with all the body parts.
2. The premotor cortex can substitute for the motor cortex to control motion. While the primary motor cortex has the largest and most powerful contribution to the function of the corticospinal tract, the premotor cortex also contributes. We know, from both anatomical and physiological studies, that there are contributions of the premotor cortex to the function of the corti-cospinal tract, but stimulation thresholds of the pre-motor cortex are higher than that of the primary motor cortex. So, while the main output of the pre-motor cortex is ordinarily to the primary motor cortex, the premotor cortex can also be the source of supraspinal control signals.
3. The contralesional hemisphere can take over motor control if all else fails. Although rather weak in humans, there are ipsilateral, corticospinal neural pathways. Although these pathways innervate many more proximal than distal muscles, they can be documented in normal humans, even in distal muscles, with the use of TMS. Such pathways are necessarily involved in recovery of patients with hemispherectomy. Although controversial, these pathways may possibly be relevant in stroke recovery. Another possible role of the undamaged hemisphere could be its interactions with the damaged hemisphere; there are transcallosal connections that are not completely characterized. Some of these transcallosal connections are inhibitory, and improvement might occur if these connections were themselves inhibited. Functional magnetic resonance imaging studies show that the damaged hemisphere has increased blood flow when bilateral movements are made; these data are consistent with the idea that activity of the undamaged hemisphere might support the damaged hemisphere. Another possibility is that the ipsilateral hemisphere helps with activity of the premotor cortex rather than the motor cortex itself.
4. Neuroplastic mechanisms can be facilitated and this is a good basis for intervention. Intensive, focused physical therapy should help restore motor function, and evidence shows that the earlier and more intensive the therapy, the better the outcome. This concept has been most fully demonstrated by the multiple successes of constraint induced (CI) movement therapy. This method forces patients to use the hemiplegic limb by constraining the good limb.

Investigations thats applied for these are, Motor Cortical (M1) plasticity with transcranial magnetic stimulation (TMS),Non-invasive brain stimulation (NBS), Repetitive transcranial magnetic stimulation (rTMS), and a few more.

Tuesday, July 9, 2013

Prosopagnosia; Face Blindness

Prosopagnosia, prosopon means face and agnosia means not knowing, also called face blindness. Face blindness is a brain disorder characterized by the inability to recognize faces.

It is thought to be the result of abnormalities, damage, or impairment in the right fusiform gyrus, a fold in the brain that appears to coordinate the neural systems that control facial perception and memory.

Face blindness can result from stroke, traumatic brain injury, or certain neurodegenerative diseases which can be of congenital reason as well. It is a disorder of face perception where the ability to recognize faces is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact. Prosopagnosia has also been associated with other disorders that are associated with nearby brain areas: left hemianopsia (loss of vision from left side of space, associated with damage to the right occipital lobe), achromatopsia (a deficit in color perception often associated with unilateral or bilateral lesions in the temporo-occipital junction) and topographical disorientation (a loss of environmental familiarity and difficulties in using landmarks, associated with lesions in the posterior part of the parahippocampal gyrus and anterior part of the lingual gyrus of the right hemisphere).

Prosopagnosia is not a unitary disorder (i.e., different people may show different types and levels of impairment), it has been argued that face perception involves a number of stages, each of which can cause qualitative differences in impairment that different persons with prosopagnosia may exhibit. The prototypical face has a specific spatial layout (eyes are always located above nose, and nose located above mouth), it is beneficial to use a holistic approach to recognize individual/specific faces from a group of similar layouts. This holistic processing of the face is exactly what is damaged in prosopagnosics. They are able to recognize the specific spatial layout and characteristics of facial features, but they are unable to process them as one entire face.


Apperceptive prosopagnosia has typically been used to describe cases of acquired prosopagnosia with some of the earliest processes in the face perception system. The brain areas thought to play a critical role in apperceptive prosopagnosia are right occipital temporal regions. People with this disorder cannot make any sense of faces and are unable to make same-different judgments when they are presented with pictures of different faces. They are unable to recognize both familiar and unfamiliar faces. However, they may be able to recognize people based on non-face clues such as their clothing, hairstyle or voice.

Associative prosopagnosia has typically been used to describe cases of acquired prosopagnosia with spared perceptual processes but impaired links between early face perception processes and the semantic information we hold about people in our memories. Right anterior temporal regions may also play a critical role in associative prosopagnosia. People with this form of the disorder may be able to say whether photos of people's faces are the same or different and derive the age and sex from a face (suggesting they can make sense of some face information) but may not be able to subsequently identify the person or provide any information about them such as their name, occupation, or when they were last encountered.

Developmental prosopagnosia(DP) is a face-recognition deficit that is lifelong, manifesting in early childhood, and that cannot be attributed to acquired brain damage. It has been suggested that a genetic factor is responsible for the condition. The term “hereditary prosopagnosia” was introduced if DP affected more than one family member, essentially accenting the possible genetic contribution of this condition. There are many developmental disorders associated with an increased likelihood that the person will have difficulties in face perception, of which the person may or may not be aware. The mechanism by which these perceptual deficits take place is largely unknown. A partial list of some disorders that often have prosopagnosiac components would include nonverbal learning disorder, Alzheimer's Disease, and autism spectrum disorders in general.

There are few neuropsychological assessments that can definitively diagnose prosopagnosia. One commonly used test is the famous faces tests, where individuals are asked to recognize the faces of famous persons. However, this test is difficult to standardize. The Benton Facial Recognition Test (BFRT) is another test used by neuropsychologists to assess face recognition skills.

Monday, July 1, 2013

A few Doctors to remember on the Doctors Day, for their contributions to make the world a Better Place.

On this day, July 1st being Doctor's Day, I would like you to have a look at the nine famous names to grace the medical profession and their achievements is short.

1. Christiaan Barnard. The South African physician served as a cardiothoracic surgeon at Groote Schuur Hospital in 1958, where he established the hospital's first heart unit. He had been experimenting for several years with animal heart transplants after he performed the first successful kidney transplant in South Africa in 1959. following the first successful kidney transplant in 1954 — Barnard performed the first kidney transplant in South Africa in 1959. Assisted by Dr. Michael DeBakey, he performed the first heart transplant in 1967. The operation lasted nine hours, and required a team of thirty people.
2. Sigmund Freud. The Austrian neurologist is renowned for inventing modern psychoanalysis, and for his groundbreaking theories of sexual symbology, dream interpretation, and the unconscious mind. He’s less well know for his career as a neurologist – he was one of the first doctors to research palsy, publishing several medical papers on the subject. Freud also believed that cocaine was a virtual cure-all, and prescribed it as a stimulant, and antidepressant, and as a cure for morphine addiction.

 3. Emil Theodor Kocher. Winner of the 1909 Nobel Prize for his work involving the thyroid gland, he founded the Kocher Institute in Berne, Switzerland. He was a pioneering researcher, and published works on antiseptic treatments, surgical infectious diseases, gunshot wounds, acute osteomyelitis, the theory of strangulated hernia, and abdominal surgery. Kocher has several instruments and surgical techniques named after him, as well as Kocher-Debre-Semelaigne syndrome.

 4. Benjamin Spock. Was the first pediatrician to study psychoanalysis as it relates to children's needs and family dynamics. After hundreds of years of child rearing that stressed discipline and obedience, Dr. Spock’s theory that parents should be more affectionate with their children and to treat them as individuals was groundbreaking, no matter how obvious it seems today.

 5. Oliver Sacks. Author of a number of popular books about his patients, the British neurologist writes very entertaining, anecdotal books that go light on the clinical details and long on the personal memoir. His most famous books are “Awakenings” (which was made into a movie starring Robert De Niro and Robin Williams) and “The Man Who Mistook His Wife for a Hat.”

6. Frederick Banting. With diabetes on the rise today, people should thank Banting on a regular basis. He, with the help of Dr. Macleod, discovered the use of insulin in the treatment of the disease.

 7. Charles F. Drew. Anyone who has ever required a blood transfusion should have great respect for Drew. An African-American doctor, his research helped improve the way we store blood, which, in turn, helped us to create the necessary blood banks for World War II. Moreover, Drew argued that blood should not be separated by donor color in blood banks.

 8. Orvan Hess. An antibiotic pioneer, Hess with another doctor successfully treated the first patient with penicillin. He went on to create a fetal heart monitor to better monitor pregnant women. His design is still the basic one used in OB units today.

 9. Joseph Lister. For years, doctors couldn't understand why wounds became infected after surgery. Lister completed a huge body of research on how infection is created, and designed many of the hygienic procedures used in hospitals today to keep infection rates to a minimum.

Sunday, June 30, 2013

Limiting yourself to the amount of salt intake will harm your health.

Salt is one of the most important nutrients, yet modern medicine has been demonizing it for decades. Now, though, even the Centers for Disease Control (CDC) must admit that they’ve had it wrong. They commissioned a study by the Institute of Medicine (IOM), and the results are clear: Reducing salt intake is almost always a bad idea.

The committee found no evidence for benefit and some evidence suggesting risk of adverse health outcomes associated with sodium intake levels in ranges approximately1,500 to 2,300 mg/day among those with diabetes, kidney disease, or CVD. The average American takes in 3,400 mg of salt a day, about 1½ teaspoons. The federal guidelines once stated that it should be brought down to less than 2,300 mg a day. It’s a good thing that people have not been following their doctors’ advice, because it would have been killing them. Low sodium intake may lead to adverse effects in people with mid- to late-stage heart failure who are receiving aggressive treatment for their disease.

At some point, you’d think that the truth about salt would sink in, but it never seems to happen. In fact, the page on which the CDC announces the new IOM report—which they
commissioned—shows absolutely no indication that there will be any rethinking of their salt reduction recommendations.

But a few of the population should keep sodium below 1,500 mg per day. Age over 51, have high blood pressure, who have severe & uncontrolled diabetes and chronic kidney diseased patients. Some evidence indicates that 1,500 to 2,300 mg of salt a day may have an adverse effect on people with diabetes, kidney disease, or heart disease.

Recent research has never documented that salt is harmful. It is, instead, a necessary nutrient. In most people, the ability to regulate salt is a simple matter that’s managed by your kidneys. Yes, too much salt is harmful, but very few people eat that amount. But public health agencies and doctors have latched onto the salt reduction mantra so firmly that it’s become equivalent to a thou-shalt-not. But it isn’t, as genuine research has shown again and again. So, it’s up to you to decide how to manage your health.

Tuesday, June 25, 2013

Miracles Of Melatonin

Can reading yourself to sleep or texting into the wee hours of the morning raise your risk of cancer?
You bet it can. Exposing yourself to artificial light at night shuts down your body’s production of an important hormone called melatonin.

Melatonin has roles in cancer prevention, strengthening your immune system, and may even slowdown cellular aging; It’s your body’s “Superhero of the Night,” and light is his number one nemesis.

For the past century or so, the developed world has been performing an open-ended experiment on itself by lengthening its days and shortening its nights in an effort to become a 24-hour per day, ever-productive society. But light pollution generated by modern technologies is taking a heavy biological toll on humans, as well as other forms of life on Earth. For more than 200,000 years, humans and other life forms evolved organs that took advantage of environmental cues. We developed a biological clock governed by Earth’s cycles of light and darkness. Artificial lighting disrupts your biological clock and melatonin production, with unfortunate effects on your health.

In humans as with all mammals, your biological clock resides in the suprachiasmatic nucleus of your brain (SCN), which is part of your hypothalamus. Based on signals of light and darkness, your SCN tells your pineal gland when it’s time to secrete melatonin. Light comes in through your eyes and travels up your optic nerves to the SCN, which is exquisitely sensitive to cycles of light and darkness.
When you turn on a light at night, you immediately send your brain misinformation about the light-dark cycle. The only thing your brain interprets light to be is day. Believing daytime has arrived, your biological clock instructs your pineal gland to immediately cease its production of melatonin. Whether you have the light on for an hour or for just a second, the effect is the same — and your melatonin pump doesn’t turn back on when you flip the light back off.

Since humans evolved in the glow of firelight, the yellow, orange and red wavelengths don’t suppress melatonin production the way white and blue wavelengths do. In fact, the range of light that inhibits melatonin is fairly narrow — 460 to 480 nm. If you want to protect your melatonin, when the sun goes down you would shift to a low wattage bulb with yellow, orange, or red light, using a salt lamp illuminated by a 5-watt bulb in this color range.

The hormone melatonin produces a number of health benefits in terms of your immune system. It’s a powerful antioxidant and free radical scavenger that helps combat inflammation. In fact, melatonin is so integral to your immune system that a lack of it causes your thymus gland, a key component of your immune system, to atrophy. Melatonin may even have a role in slowing the aging of your brain. In addition to helping you fall asleep and bestowing a feeling of overall comfort and well being, melatonin has proven to have an impressive array of anti-cancer benefits. Melatonin inhibits the proliferation of a wide range of cancer cell types, as well as triggering cancer cell apoptosis (self destruction). The hormone also interferes with the new blood supply tumors require for their rapid growth (angiogenesis). Melatonin can boost efficacy and decrease the toxicity of cancer chemotherapy.

Glioblastoma is a nasty, aggressive form of brain cancer with a poor prognosis and not much in the way of effective treatments. However, melatonin may offer some hope. patients with a glioblastoma were given either radiation and melatonin, or radiation alone. Twenty-three percent of the patients receiving the melatonin were alive one year later, while none who received radiation alone were still alive. Another study found that melatonin reduced the growth of prostate cancer. Studies show similarly encouraging results for lung, pancreatic, colorectal and other types of cancer.

Two common environmental "noise" factors that can make sleep elusive are light pollution and temperature. The following suggestions can improve your sleep hygiene and help you optimize your melatonin production.

*.Avoid watching TV or using your computer in the evening, at least an hour or so before going to bed. These devices emit blue light, which tricks your brain into thinking it’s still daytime. Normally your brain starts secreting melatonin between 9 and 10 pm, and these devices emit light that may stifle that process.

*.Make sure you get BRIGHT sun exposure regularly. Your pineal gland produces melatonin roughly in approximation to the contrast of bright sun exposure in the day and complete darkness at night. If you are in darkness all day long, it can’t appreciate he difference and will not optimize your melatonin production.

*.Sleep in complete darkness, or as close to it as possible. Even the slightest bit of light in your bedroom can disrupt your biological clock and your pineal gland's melatonin production. Even the tiniest glow from your clock radio could be interfering with your sleep, so cover your radio up at night or get rid of it altogether. Move all electrical devices at least three feet away from your bed. You may want to cover your windows with drapes or blackout shades.

*.Install a low-wattage yellow, orange or red light bulb if you need a source of light for navigation at night. Light in these bandwidths does not shut down melatonin production in the way that white and blue bandwidth light does. Salt lamps are handy for this purpose.

*.Keep the temperature in your bedroom no higher than 70 degrees F. Many people keep their homes too warm (particularly their upstairs bedrooms). Studies show that the optimal room temperature for sleep is between 60 to 68 degrees.
*.Take a hot bath 90 to 120 minutes before bedtime. This increases your core body temperature, and when you get out of the bath it abruptly drops, signaling your body that you are ready to sleep.
*.Avoid using loud alarm clocks. Being jolted awake each morning can be very stressful. If you are regularly getting enough sleep, you might not even need an alarm.

*.Get some sun in the morning, if possible. Your circadian system needs bright light to reset itself. Ten to 15 minutes of morning sunlight will send a strong message to your internal clock that day has arrived, making it less likely to be confused by weaker light signals during the night. More sunlight exposure is required as you age.
*.Be mindful of electromagnetic fields in your bedroom. EMFs can disrupt your pineal gland and its melatonin production, and may have other negative biological effects as well. A gauss meter is required if you want to measure EMF levels in various areas of your home.

An Scientific Theory on Why Fixation of Males lies of Females Bosoms.

Why do men devote so much headspace to those big, bulbous bags of fat drooping from women's chests? Scientists have never satisfactorily explained men's curious breast fixation, but now, neuroscientists has struck upon an explanation human evolution has harnessed an ancient neural circuit that originally evolved to strengthen the mother-infant bond during breast-feeding, and now uses this brain circuitry to strengthen the bond between couples as well. The result? Men, like babies, love breasts.

When a woman's nipples are stimulated during breast-feeding, the neurochemical oxytocin, otherwise known as the "love drug," floods her brain, helping to focus her attention and affection on her baby. But research over the past few years has shown that in humans, this circuitry isn't reserved for exclusive use by infants. nipple stimulation enhances sexual arousal in the great majority of women, and it activates the same brain areas as vaginal and clitoral stimulation. When a sexual partner touches, massages or nibbles a woman's breasts, this triggers the release of oxytocin in the woman's brain, just like what happens when a baby nurses. But in this context, the oxytocin focuses the woman's attention on her sexual partner, strengthening her desire to bond with this person. In other words, men can make themselves more desirable by stimulating a woman's breasts during foreplay and sex. Evolution has, in a sense, made men want to do this.

Attraction to breasts is a brain organization effect that occurs in straight males when they go through puberty, Evolution has selected for this brain organization in men that makes them attracted to the breasts in a sexual context, because the outcome is that it activates the female bonding circuit, making women feel more bonded with him. It's a behavior that males have evolved in order to stimulate the female's maternal bonding circuitry.

Thursday, February 28, 2013

The Legend of Hippolyte

In Greek mythology, Hippolyta, Hippoliyte, or Hippolyte was the Amazonian queen who possessed a magical girdle she was given by her father Ares, the god of war. The girdle was a waist belt that signified her authority as queen of the Amazons. She figures prominently in the myths of both Heracles and Theseus. As such, the stories about her are varied enough that they may actually be about a few different characters.

Versions of the myth

In the myth of Heracles, Hippolyta’s girdle was the object of his ninth labor. He was sent to retrieve it for Admeta, the daughter of king Eurystheus. Most versions of the story say that Hippolyta was so impressed with Heracles that she gave him the girdle without argument, perhaps while visiting him on his ship. But then (according to Apollodorus) the goddess Hera, making herself appear as one of the Amazons, spread a rumor among them that Heracles and his crew were actually abducting their queen. So the Amazons attacked the ship. In the fray that followed, Heracles slew Hippolyta, stripped her of the belt, fought off the attackers, and sailed away.

In the myth of Theseus, the hero joined Heracles in his expedition, or went on a separate expedition later, and was actually the one who had the encounter with Hippolyta. Some versions say he abducted her, some that Heracles did the abducting but gave her to Theseus as spoils, and others that she fell in love with Theseus and betrayed the Amazons by willingly leaving with him. In any case, she was taken to Athens where she was wed to Theseus, being the only Amazon to ever marry. In some renditions the other Amazons became enraged at the marriage and attacked Athens. This was the Attic War, in which they were defeated by Athenian forces under Theseus or Heracles. In other renditions Theseus later put Hippolyta aside to marry Phaedra. So Hippolyta rallied her Amazons to attack the wedding ceremony. When the defenders closed the doors on the attackers, Hippolyta was killed. Or Theseus directly killed her in the fight. Or she was accidentally killed by another Amazon, Molpadia, while fighting by Theseus’ side, or was accidentally killed by her sister Penthesilea during this battle or in a separate incident. This killer was in turn slain by Theseus or Achilles. But some stories paint Theseus in a more favorable light, saying that Hippolyta was dead before he and Phaedra were wed and so this battle didn’t occur. Further complicating the narratives, a number of ancient writers say the Amazon in question wasn’t Hippolyta at all but her sister Antiope, Melanippe or Glauce. Moreover, there are combined versions of the tale in which Heracles abducts and kills Hippolyta while Theseus (assisted by Sthenelus and Telamon) abducts and marries Antiope. There are also stories that Hippolyta or Antiope later bore Theseus a son, Hippolytus.

Dual Star "Papaya"

Saturday, February 9, 2013

A Star "Papaya" !

Greek Godess Of Peace

EIRENE (or Irene) was the goddess of peace (eirĂȘnĂȘ) and of the season of spring (eiar, eiarinos). Late spring was the usual campaign season in Greece when peace was most at risk. Eirene was one of three Horai, goddesses of the seasons and the keepers of the gates of heaven. Her sisters were Eunomia (Order or Good-Pasture) and Dike (Justice). She was probably identified with the Hora Thallo (Green Shoots), whose name Hesiod gives to Eirene as an epithet in the Theogony. Her opposite number was Polemos (War). In classical art she usually appears in the company of her two sister Horai bearing the fruits of the seasons. Statues of the goddess represent her as a maiden holding the infant Ploutos (Wealth) in her arms. In this guise she was identified with Demeter and Tykhe.