Alfa (huruf : Α, α) is the first Greek alphabet.


Derived from the Latin Language Neo means New


My last name from my parents. Literally A New One.

Pheromon : Falling in Love (From Your Nose then Going Down to Your Heart)

Sunday, January 30, 2011

The bulk majority of human pheromones belong to a group of chemicals known as 16-androstenes.
The term pheromone - from the Greek roots of pherin, to transfer, and hormone, to excite - describes a class of chemicals that are communicated between animals of the same species and that elicit stereotyped behavioural or neuroendocrine responses. Some pheromones - called "releaser" pheromones - elicit an immediate response, while others - termed "primer" pheromones - induce long-term changes in behavioural or endocrine state.

Pheromone-induced responses are mediated primarily by the vomeronasal organ (VNO). The VNO, also known as "Jacobson's organ", is part of an accessory olfactory system. It is present in a variety of non-human vertebrates but its existence in the human has been open to question until recently.

Historical Perspective
The VNO was first discovered by Ruysch (1703), a military doctor, in a soldier with a facial wound. The organ was named after Jacobson who published his findings on animals, but not humans, in 1811. Various other investigators have published studies; Potiquet (1891) observed the VNO in 25% of 200 adult humans, Pearlman (1934) described its occurrence in many animals, in human embryos and mentioned that it may be found occasionally in the adult human. (more detail can be found in Moran, Monti-Bloch, Stensaas and Berliner (1994)).

It was work published by Crosby and Humphrey (see below) that put the functional presence of the VNO in the human adult into doubt. In a standard anatomical textbook, "Correlative Anatomy of the Nervous System" by Crosby, Humphrey and Lauer (1962), we read the following; "In some human embryos, an accessory olfactory bulb, with complete representation of layering from the glomerular through the mitral cell layer, is to be found on the dorsomedial aspect of the main olfactory bulb (Humphrey, 1940). The accessory bulb receives the vomeronasal (or Jacobson's) nerve from the vestigial vomeronasal organ, which has also been demonstrated in the human embryo (McCotter, 1912). The vomeronasal nerve and its associated bulb vary in size and may be absent in the human embryo (Humphrey, 1940; Macchi, 1951). This variability appears to be characteristic of these structures in certain other adult primates (Lauer, 1945, 1949) Jacobson's organ and nerve and the accessory olfactory bulb are well developed in certain submammals and some subprimate mammals (Crosby and Humphrey, 1939). They are not present in adult man (Crosby and Humphrey, 1941). In human development these structures are merely ontogenetic signs of the persistence of phylogenetic structures and are without function".

Largely as a result of the above observations the existence of the VNO in humans has been disregarded. The consensus has been that, if it exists at all, it is vestigal and not functional. As recently as 1991 a paper by Meredith asserted that the accessory olfactory system is not present in humans or other old-world primates. This disregard for the existence of the VNO in adult humans is exemplified by the fact that the area containing the VNO is often removed during plastic surgery on the nose.

In 1980, Kreutzer and Jafek documented the early morphogenesis of the vomeronasal organ in the human embryo and early foetus. Later, in 1985, Johnson et al. examined 100 human adults specifically for the presence of the opening of the vomeronasal organ on the antero-interior part of the nasal septum. This was found in 39% of patients. Twenty seven human septums were removed post mortem, and vomeronasal structures were found in 70% of these. However, histological examination failed to reveal any evidence that these organs were functional (Johnson et al., 1985). In the same year, Nakashima et al. studied the VNO and nerves of Jacobson in a 28-week human foetus. They described the structure of the organ and traced the vomeronasal nervealong the nasal septum and through the cartilaginous cribriform plate with the olfactory nerve. While they found evidence for the existence of receptors in the vomeronasal epithelium similar to those in the olfactory epithelium, they suggested that the lack of intraepithelial blood vessels and mitotic figures in the epithelium indicated that the organ was undergoing degeneration at 28 weeks of gestation (Nakashima, Kimmelman and Snow, 1985). Since 1985 there has been a steady accumulation of evidence demonstrating the presence of the VNO in most, if not all, humans (Moran et al., 1985, 1991; Johnson et al., 1985; Stensaas et al., 1991; Garcia-Velasco and Mondragon, 1991, and reviewed in Moran et al., 1995).

The VNO is located bilaterally on the anterior third of the floor of the nasal septum. It opens into the nasal cavity by a pit which varies in size from 0.2 to 2 mm situated 1-2 cm from the posterior margin of the nostril. 

VNO Structure
The VNO is lined by a pseudostratified, columnar epithelium some 60um in depth that lies on a thick basement membrane. The vomeronasal neuroepithelium contains three morphologically distinct cell types; basal cells, dark cells and light cells. The basal cells are small, polygonal, dark-staining cells, measuring 6um in diameter. The dark cells are tall, slender, columnar cells with densely staining cytoplasm. The light cells are tall, columnar cells that, like the dark cells, extend from the basement membrane to the free surface of the epithelium. They differ from the surrounding cells of the respiratory epithelium in the nose by having no cilia (Moran et al, 1995).

VNO Receptors
The vomeronasal organ in the human foetus from 12 to 23 weeks is lined by a pseudostratified epithelium, with neurone-specific enolase (NSE) positive cells which resemble olfactory receptors. However, at 36 weeks the organ was lined by a respiratory epithelium and did not show any receptor-like cells, although there were some pear-shaped NSE-positive cells in the upper part of the respiratory epithelium of unknown significance (Boehm and Gasser, 1993). It was suggested that, during the early foetal period, the VNO could have some, as yet unknown, sensory function (op. cit.).

In contrast, calbindin, a 28Kd protein that has been immunolocalised to VNO receptor cells, was found to be expressed in humans, firstly in a male neonate and secondly an adult female suggesting the presence of receptors during early development and in the adult (Johnson, Eller and Jafek, 1994)

Whether or not the VNO continues to express receptor cells or neuronal markers in the adult, the structure itself continues to expand according to Smith et al. (1997). When comparing the increase in length of the VNO in the developing foetus to the length in the adult human, they concluded that further prenatal or postnatal size increase must occur.
VNO - Functionality
Compounds occurring naturally on the human skin were found to cause a local depolarisation when applied directly to the VNO (Monti-Bloch and Grosser, 1991). The nature of these compounds was not disclosed. This depolarisation had the characteristics of a receptor potential. Furthermore these compounds did not cause a response from the olfactory epithelium and, olfactory stimulants (e.g. cineole) had no effect on the VNO. Using the same compounds sexual dimorphism was demonstrated in their effect on electrodermal activity (Monti-Bloch et al, 1994). These compounds were subsequently revealed to be 16-androstenes and estrenes (Berliner, 1993; 1994). The androstenes have been previously isolated from human sweat (secreted by the axillary apocrine glands) (Gower et al., 1985).
Another "vomeropherin", pregna-4,20-diene-3,6-dione (PDD), caused evoked potentials in the VNO and also changed gonadotropin pulsatility in males, resulting in a reduced level of luteinizing hormone (Berliner et al, 1996) and testosterone (Monti-Bloch et al, 1998). In addition, PDD decreased respiratory frequency, increased cardiac frequency and caused event-related changes of electrodermal activity in EEG pattern (Berliner et al, 1996). 

Is The Adult Human VNO Vestigial?
The overwhelming anatomical evidence suggests that the in the adult human the VNO is vestigial (Meredith, 2001). There is no evidence for any anatomical connection from the VNO to the brain. Furthermore, the channel responsible for pheromone transduction in lower mammals, TRP2 (a non-selective cation channel), is a pseudogene in humans. However, this does not mean that human pheromones do not exist. mRNA for a vomeronasal receptor, hV1RL1, has been found in the human olfactory epithelium (Rodriguez & Mombaerts, 2002).

Human Pheromones
When pheromones were first discovered in the late 1950s they were defined as “..substances which are secreted to the outside by an individual and received by a second individual of the same species, in which they release a specific reaction, for example, a definite behaviour or a developmental process” (Karlson and Luscher, 1959).
Following the pioneering work on menstrual synchrony by McClintock (1971), Stern and McClintock (1998) have shown that odourless axillary compounds from the armpits of women in the late follicular phase of their menstrual cycles accelerated the preovulatory surge of luteinizing hormone of recipient women and shortened the menstrual cycles. Axillary compounds from the same donors which were collected later in the menstrual cycle (at ovulation) had the opposite effect: they delayed the luteinizing hormone surge of the recipients and lenghtened their menstrual cycle (Stern and McClintock, 1998).
The work by McClintock is very supportive of the existence of a chemical signal in axillary secretion - a pheromone - but it does not prove the existence of a functional VNO. 

Androstadienone is the current best candidate we have for a human pheromone. Is is a component of human (in particular male) secretions. Does androstadienone meet Karlson & Luscher (1959) "pheromone" criteria? In human studies in which androstadienone had access to the olfactory mucosa both physiological and psychological effects have been reported (Jacob and McClintock, 2000; Jacob, Hayreh and McClintock, 2001; Jacob, Garcia, Hayreh and McClintock, 2002 Bensafi et al., 2003; Lundstrom et al., 2003; Bensafi et al 2004a, 2004b; Cornwell et al., 2004). While none of these changes can be regarded as the behavioural changes required for a compound to qualify as a pheromone, Savic et al. (2001) demonstrated that androstadienone activated the hypothalamus in a gender-specific manner (it activated the hypothalamus in women but not men). Compared with other odorous substances, androstadienone activated the anterior part of the inferior lateral prefrontal cortex (PFC) and the superior temporal cortex (STP) in addition to olfactory areas (Gulyas et al., 2004). The PFC and STP have been implicated in aspects of attention, visual perception and recognition and social cognition.

The definition of a pheromone (see above, Karlson and Luscher 1959) was later modified to include a mutual benefit requirement (Rutowski, 1981). In this context it is possible to see such mutual benefit if the pheromone leads, for example, to choice of partner on the basis of their HLA-dependent odortype to increase immune diversity (Ober et al., 1997, 1999) and lower miscarriage rates (Ober et al., 1998) or if the pheromone participates in the mother-infant bonding process (Schleidt, 1992). On its own it is unlikely to be able to achieve these outcomes but, as recently reported by Coureaud et al (2004), a pheromone can act as a reinforcing agent or a one-trial conditioning agent in which the presence of the pheromone converts a second odour (that of the partner or infant) into a conditioned stimulus.

Odor and Major Histocompatibility Complex
Mice can distinguish one another by odour. This odour is genetically determined and partly specified by the H-2 major histocompatibility complex (MHC) (Yamazaki et al, 1979; 1994) on chromosome 17 (Schellinck et al, 1993). There are however other genetic loci coding for odortypes found on the nonrecombining part of the Y chromosome (Schellinck et al, 1993). These odors are excreted in the urine and may play a part in pregnancy block (the Bruce effect), aggression and other mouse social behaviours.

The human equivalent of the MHC locus is the human leucocyte antigen (HLA). Numerous studies have been carried out with humans that suggest that axillary odour contains enough chemical differences in its odour profile to allow for discrimination between individuals. It has been hypothesised that at least some of this individual specific odour may be under the control of human leucocyte antigen (HLA) genes (Preti, Spielman and Wysocki, 1997). Studies have shown that women prefer those male odours that have HLA types different from their own - a preference that was reversed when those women doing the rating were taking oral contraceptives.
Supporting evidence for the existence of individual-specific odour comes from studies in which mothers have identified their own newborn infants from the smell of a previously worn T-shirt (Schaal et al, 1980). In turn, infants prefer breast or axillary pads from their own mothers, distinguishing the odour from other kin (Schaal et al, 1991).

Pheromones are well established in many species but the their existence in humans is still controversial. Much of the problem lies with the fact that the original definition of a pheromone cannot allow for volitional control over the biological response. Humans have a will of their own and can refuse the biological imperative. How then do you determine if a chemical signal is altering human behaviour? The experiments that have attempted to do this, e.g. by measuring autonomic responses, have had extremely variable results. The results in one lab are different to those in another. This implies that the are too many uncontrolled variables. Humans are obstinately different. They respond differently depending upon whether the experimenter is male or female for instance!
While the behavioral changes induced by axillary secretions are supportive evidence, they have not convinced everyone in the field - measuring menstrual synchrony is a process fraught with problems. Receptors (or at least their mRNA) for pheromones have been found in the human olfactory epithelium, but we are still waiting for someone to demonstrate the presence of a pheromone receptor protein expressed in the surface membrane of an olfactory receptor neuron and that responds to a ligand (a potential pheromone) - as has been demonstrated for the olfactory receptors.

History of Bullet Proof Vest

Body Armor in Middle Age at England
The principle of bullet-proof armor has been developed since the early Middle Ages. Starting from the knight  with iron armor, which can reduce puncture wounds sword or shooting an arrow. Unfortunately with the development of firearms, the protection becomes useless.

Aramid (Kevlar)
This material was found in 1964, by Stephanie Kwolek, an American chemist, who worked as a researcher at the DuPont company.

Stephanie Kwolek
Aramid is stand for aromatic polyamide. Aramid has a strong structure, tough, has a good impact and also vibration damping, acid and alkaline resistant and besides that can be heated up to 370°C (so is not flammable). Because of that advantages, aramid is also used in the aircraft, tanks, and aerospace (rocket). The products was known as Kevlar. Kevlar is light, and 5 times stronger than steel.

Structure Molecule of Aramid
This fiber is commonly known as Kevlar™ 

The thickness of Kevlar layer is less than 1 mm, generally in standard body armor, it contain up to 32 layers and the weight can reach 10 kg.
Basic Principle of Bullets Proof Vest
The basic principle of bullets proof vest is reduce as much as possible of kinetic energy of the bullet, by using layers of kevlar, it can absorb energy, so that energy is not enough anymore to make a bullet break through the vest. In absorbing the kinetic energy of bullet, Kevlar will deformed inwards and it will be transferred into the pressure to the user's body. The maximum limit pressure should not be more than 4.4 cm (44 mm). If that limit is exceeded, the user will have internal organs injury, which is very dangerous.
Bullet Strike in Bullet Proof Vest

Kevlar Deformation

This analogy like goal's net which can hold the kinetic energy of moving ball. The net is contain thight structure of the rope. If the moving ball go through the net, the kinetic energy of the ball will absorb by the net and the rope around will extending and the pressure of the rope will discarged the goal post.
The picture above show if the bullet proof armor can fully protect the user but sometime if user is not lucky, something bad will happen. The main purpose of bullet proof armor is only decrease the kinetic energy from the moving bullet then the user will not dead. No matter because of this reducing pressure from bullet, the user will suffer blunt force trauma or broken bone.

Bullet Proof Vest or Ballistic Vest ? 
Bullet Proof Vest divided by Soft Body Armor and Hard Body Armor.

Soft Body Armor
Soft Body Armor type 1
Soft Body Armor type 2
In everyday duty of cop / detective in undercover work prefers a lightweight bulletproof clothing like that. Soft body armor is now mostly made of Aramid Fibers.

Hard Body Armor
Hard Body Armor
Hard body armor is like soft body armor but it adding with several special layer. The layer that used is ceramic (Al2O3 "Alumina"), metal slab, or composite. The weight is heavy and thick and uncomfortable, so no matter is rarely used in daily duty. It only use in high risk duty like military operation or SWAT team operation.

SWAT Team Operation
Standart Level of The Type of Bullet Proof Armor
Standard measurement of bullet proof armor commontly is using NIJ Standart (National Institute of Justice) in America. In this standard, bullet proof armor can devided by several level which is :
  • Level I, 
  • Level II-A, 
  • Level II, 
  • Level III-A, 
  • Level III, and 
  • Level IV. 
Level I is the lowest level. This armor only proofing low caliber bullet.
Level of Bullet Proof Armor
Type of bullet and which level that can protect the user

With using new composite material, the safety level is increasing time by time. But it still have the weakness that is "If you want to safe, use the thick one, but you must carrying that heavy vest". For this condition, the scientist and the military always create new product which is lighter and stronger.

pH of Your Food. Is It Acid or Alkaline?

Saturday, January 29, 2011

pH Meter for Food
A surprising number and variety of physical problems and diseases can be caused by the problem of foods that are acid-producing after digestion. Today the vast majority of the populace in industrialized nations suffers from problems caused by the stress of acidosis, because both modern lifestyle and diet promote acidification of the body's internal environment.

The current typical Western or Eastern diet is largely composed of acid-forming foods (proteins, cereals, sugars). Alkaline-producing foods such as vegetables are eaten in much smaller quantities. Stimulants like tobacco (cigarette), coffee, tea, and alcohol are also extremely acidifying. Stress, and physical activity (both insufficient or excessive amounts) also cause acidification.

Many foods are alkaline-producing by nature, but manufactured processed foods are mostly acid-producing. It is important to consume at least 60% alkaline-producing foods in our diet, in order to maintain health. We need plenty of fresh fruits and particularly vegetables (alkaline-producing) to balance our necessary protein intake (acid-producing). And we need to avoid processed, sugary or simple-carbohydrate foods, not only because they are acid-producing but also because they raise blood sugar level too quickly (high glycemic index therefore fattening); plus they tend to be nutrient-lacking and may be toxic too.

The body maintains correct pH in the blood at all costs, by homeostasis, but that is stressful for the body's systems and resources when the diet is unbalanced in terms of acid-forming foods (the residue after digestion, that is). Within cells it's a different story. Saliva and urine tests show clearly enough the changes in alkalinity or acidity that are caused by diet and lifestyle.

What is the body's pH?
Water is the most abundant compound in the human body, comprising 70% of the body. The body therefore contains a wide range of solutions, which may be more or less acid. pH (potential of Hydrogen) is a measure of the acidity or alkalinity of a solution - the ratio between positively charged ions (acid-forming) and negatively charged ions (alkaline-forming.) The pH of any solution is the measure of its hydrogen-ion concentration. The higher the pH reading, the more alkaline and oxygen rich the fluid is.  The lower the pH reading, the more acidic and oxygen deprived the fluid is. The pH range is from 0 to 14, with 7.0 being neutral.  Anything above 7.0 is alkaline, anything below 7.0 is considered acidic.

Human blood pH should be slightly alkaline (7.35 - 7.45). Below or above this range means symptoms and disease. If blood pH moves below 6.8 or above 7.8, cells stop functioning and the body dies. The body therefore continually strives to balance pH. When this balance is compromised many problems can occur.

An imbalanced diet high in acidic-producing foods such as animal protein, sugar, caffeine, and processed foods puts pressure on the body's regulating systems to maintain pH neutrality. The extra buffering required can deplete the body of alkaline minerals such as sodium, potassium, magnesium, and calcium, making the person prone to chronic and degenerative disease. Minerals are borrowed from vital organs and bones to buffer (neutralize) the acid and safely remove it from the body. Because of this strain, the body can suffer severe and prolonged damage--a condition that may go undetected for years.

pH Range
Test Your Body's Acidity or Alkalinity with pH Strips
It is recommended that you test your pH levels to determine if your body's pH needs immediate attention. By using pH test strips (Litmus Paper), you can determine your pH factor quickly and easily in the privacy of your own home. The best time to test your pH is about one hour before a meal and two hours after a meal.

Saliva pH Test:
Simply wet a piece of Litmus Paper with your saliva. While generally more acidic than blood, salivary pH mirrors the blood and tells us what the body retains. It is a fair indicator of the health of the extracellular fluids and their alkaline mineral reserves. The optimal pH for saliva is 6.4 to 6.8. A reading lower than 6.4 is indicative of insufficient alkaline reserves. After eating, the saliva pH should rise to 7.5 or more. To deviate from an ideal salivary pH for an extended time invites illness. If your saliva stays between 6.5 and 7.5 all day, your body is functioning within a healthy range.
Acidosis, an extended time in the acid pH state, can result in rheumatoid arthritis, diabetes, lupus, tuberculosis, osteoporosis, high blood pressure, most cancers and many more.  If salivary pH stays too low, the diet should focus on fruit, vegetables and mineral water as well as remove strong acidifiers such as sodas, whole wheat and red meat.

Urine pH Test:
The pH of the urine indicates how the body is working to maintain the proper pH of the blood. The urine reveals the alkaline (building - anabolic) and acid (tearing down - catabolic) metabolic cycles. The pH of urine indicates the efforts of the body via the kidneys, adrenals, lungs and gonads to regulate pH through the buffer salts and hormones. Urine can provide a fairly accurate picture of body chemistry, because the kidneys filter out the buffer salts of pH regulation and provide values based on what the body is eliminating. Urine pH can vary from around 4.5 to 9.0 in extremes, but the ideal range is 6.0 to 7.0. If your urinary pH fluctuates between 6.0 to 6.5 first thing in the morning and between 6.5 and 7.0 in the evening before dinner, your body is functioning within a healthy range.
Urine testing may indicate how well your body is excreting acids and assimilating minerals, especially calcium, magnesium, sodium and potassium. These minerals function as "buffers." Buffers are substances that help maintain and balance the body against the introduction of too much acidity or too much alkalinity. Even with the proper amounts of buffers, acid or alkaline levels can become stressful to the body's regulatory systems. When the body produces too many of these acids or alkalis, it must excrete the excess. The urine is the method the body uses to remove any excess acids or alkaline substances that cannot be buffered. If the body's buffering system is overwhelmed, a state of "auto-intoxication" exists, and attention should be given to reducing this stress.

Use the food charts to the right and below to make your lifestyle more alkaline and reap the benefits of vibrant health and abundant energy.
pH of Food
It is important that your daily dietary intake of food naturally acts to balance your body pH. To maintain health, the diet should consist of at least 60% alkaline forming foods and at most 40% acid forming foods. To restore health, the diet should consist of 80% alkaline forming foods and 20% acid forming foods.

Positive Aspects of Nicotine Use

Thursday, January 27, 2011

Nicotine can be found in tobacco. Tobacco is generally use to make a cigarette.

Dried Tobacco
Do you know that is several positive effect from smoking cigarette? We usually showed many of attention word in the cigarette there are "Smoking can caused cancer, heart attack, impotent, and bad effect of pregnancy". But, I found positive aspects of nicotine use. They are for emotional and physiologist, for lower blood pressure. For further information, you can see below :
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Chillis, Capsaicin, and Scoville

Chilli is hot. Chilli can make burning sensasion. Many kind of species of chilli in the world. But in this cause I will tell you about :
  1. Capsaicin
  2. Scoville
  3. Chilli by Zero Scoville Heat Units

 is the active component of chili peppers, which are plants belonging to the genus Capsicum. It is an irritant for mammals, including humans, and produces a sensation of burning in any tissue with which it comes into contact. Capsaicin and several related compounds are called capsaicinoids and are produced as a secondary metabolite by chili peppers, probably as deterrents against certain herbivores and fungi. Pure capsaicin is a hydrophobic, colorless, odorless, crystalline to waxy compound.
Capsaicin compound was first extracted (albeit in impure form) in 1816 by Christian Friedrich Bucholz (1770–1818). He called it "capsicin," after the genus Capsicum from which it was extracted. Capsaicin was first isolated in pure, crystalline form in 1876 by John Clough Thresh (1850–1932), who gave it the name "capsaicin". In 1873 German pharmacologist Rudolf Buchheim (1820–1879) and in 1878 the Hungarian doctor Endre Hőgyes stated that "capsicol" (partially purified capsaicin) caused the burning feeling when in contact with mucous membranes and increased secretion of gastric juice. The structure of capsaicin was partly elucidated by E. K. Nelson in 1919. Capsaicin was first synthesized in 1930 by E. Spath and S. F. Darling. In 1961, similar substances were isolated from chili peppers by the Japanese chemists S. Kosuge and Y. Inagaki, who named them capsaicinoids.
Capsaicin is present in large quantities in the placental tissue (which holds the seeds), the internal membranes and, to a lesser extent, the other fleshy parts of the fruits of plants in the genus Capsicum. The seeds themselves do not produce any capsaicin, although the highest concentration of capsaicin can be found in the white pith around the seeds. The seeds of Capsicum plants are predominantly dispersed by birds. Birds do not have the receptor to which capsaicin binds, so it does not function as an irritant for them. Chili pepper seeds consumed by birds pass through the digestive tract and can germinate later, but mammals have molars, which destroy seeds and prevent them from germinating. Thus, natural selection[citation needed] may have led to increasing capsaicin production because it makes the plant less likely to be eaten by animals that do not help it reproduce. There is also evidence that capsaicin evolved as an anti-fungal agent, and capsaicinoids are broadly anti-microbial. In 2006, it was discovered that tarantula venom activates the same pathway of pain as is activated by capsaicin, the first demonstrated case of such a shared pathway in both plant and animal anti-mammal defense.
Here, 10 things you should know about capsaicin:
1.Capsaicin is the active component of chili peppers.
Capsaicin is actually an irritant to humans, producing a burning sensation in any tissue it touches. Capsaicin works by depleting or interfering with substance P, a chemical involved in transmitting pain impulses to the brain. The properties of capsaicin make it an option for relieving pain associated with osteoarthritis, rheumatoid arthritis, and diabetic neuropathy. Capsaicin is used to relieve muscle pain, joint pain, or nerve pain.

2.Capsaicin is available over the counter.
You do not need a prescription for capsaicin from your doctor. You can find products containing capsaicin in your drugstore for over-the-counter purchase. You should follow the directions given by your doctor or the directions on the label (there are different dosages or strengths of capsaicin available). For pain relief, capsaicin is usually used 3 or 4 times a day. You should rub the capsaicin cream or gel into the painful area until no more cream is visible on the skin.

Wash hands thoroughly after applying capsaicin to other areas of the body. If the capsaicin was applied for hand pain, however, wash your hands after 30 minutes.
3.Don't use extra doses of capsaicin.
Stick to the directions, but if you should inadvertently miss a dose, use it as soon as you remember -- unless it's close to the time of the next dose.
4.Capsaicin has no known drug interactions.Though there are no recognized drug interactions with capsaicin, ask your doctor to be sure that you can use capsaicin, and continue to take your current medications. It's important to inform your doctor about any products you are using.
5.Capsaicin may cause a burning sensation.
You will likely experience a warm, burning, stinging sensation when you begin using capsaicin. The sensation, which is expected when beginning use, may actually continue for 2 to 4 weeks. The sensation should lessen the longer you use capsaicin. Reducing the number of daily doses of capsaicin will not reduce the sensation, but it may reduce the pain relief achieved.
6.Arthritis pain relief is not immediate.
Even with regular use of capsaicin, arthritis pain relief will take some time. Pain relief from arthritis typically is evident 1 to 2 weeks after starting capsaicin. To prevent pain from returning, capsaicin must be continued. However, if pain is not better after using capsaicin for 3 or 4 weeks, talk to your doctor. It may not be worth it to continue.
7.Capsaicin must be handled with care.Be aware of what can happen if you get capsaicin in your eyes or on other sensitive body parts because of the burning sensation it causes. If capsaicin gets in your eyes, immediately flush your eyes with water. To rid other sensitive areas of capsaicin and the burning feeling, wash the areas with warm soapy water. Keep capsaicin out of reach of children.
8.Some people should not use capsaicin.There are warnings about using capsaicin under certain circumstances. Before using capsaicin, tell your doctor about:

    * broken skin
    * skin irritation
    * previous allergic reactions to capsaicin, hot peppers, other drugs, dyes, foods, preservatives
    * breastfeeding
    * pregnancy or current attempts to become pregnant

Also, be aware that capsaicin should not be used by children under 2 years of age.
9.Research supports use of capsaicin for osteoarthritis and rheumatoid arthritis.A study from 1991 involved 70 osteoarthritis patients and 31 rheumatoid arthritis patients. Patients were instructed to apply 0.025% capsaicin or placebo to painful knees, four times a day. Results revealed that 80% of patients treated with capsaicin experienced pain reduction following two weeks of treatment. 
10.Research also supports the use of capsaicin for osteoarthritis of the hands.Capsaicin 0.075% was evaluated for osteoarthritis and rheumatoid arthritis in a 4-week study, published in 1992. All of the study participants had significant hand pain and applied capsaicin to their hands 4 times daily. It was found that capsaicin reduced tenderness and pain in osteoarthritis of the hand patients, but not rheumatoid arthritis patients when compared to placebo. 

The Scoville scale is a measurement of the spicy heat (or piquance) of a chili pepper. The number of Scoville heat units (SHU) indicates the amount of capsaicin present. Capsaicin is a chemical compound that stimulates chemoreceptor nerve endings in the skin, especially the mucous membranes. The scale is named after its creator, American chemist Wilbur Scoville. His method, devised in 1912, is known as the Scoville Organoleptic Test. The modern commonplace method for quantitative analysis uses high-performance liquid chromatography, making it possible to directly measure capsaicinoid content.

The chilis with the highest rating on the Scoville scale exceed one million Scoville units, and include specimens of naga jolokia or bhut jolokia and its cultivars, the "Dorset naga" and the "Ghost chili," neither of which has official cultivar status. The Naga Viper currently holds the unofficial title for hottest pepper. It was produced in the UK by crossing the three hottest peppers known to the world, including the Bhut jolokia. Researchers at Warwick University tested the Naga Viper and found that it measures 1,359,000 on the Scoville scale. It should be noted that a chilli trial carried out by a team from the BBC's Gardeners' World programme put the heat value of Dorset Naga at a staggering 1.6 million SHU. Those levels were tested by Warwick HRI. However, this is not the average Scoville Heat Unit level of the pepper, nor was this submitted to any world record holder. Numerical results for any specimen vary depending on its cultivation conditions and the uncertainty of the laboratory methods used to assess the capsaicinoid content.
Chilli by Zero Scoville Heat Units
Bell Pepper, Cubanelle, Aji Dulce ( have 0 point of SHU )
Bell Pepper


Aji Dulce (They're sweet, not spicy)

Bayesian-LOPA Methodology Development for LNG Industry

Thursday, January 6, 2011

In order to meet the fast growing LNG (Liquefied Natural Gas) demand, many LNG importation terminals are operating currently. Thus, it is important to estimate the potential risks in LNG terminals with LOPA (Layer of Protection Analysis) which can provide quantified results with less time and efforts than other methods. For LOPA application, failure data are essential to compute risk frequencies. However, the failure data from the LNG industry are very sparse and have statistically shake grounds. Therefore, Bayesian estimation, which can update the generic data with plant specific data, was used to compensate for its weaknesses.  

Based on Bayesian estimation, the frequencies of initiating events were obtained using a conjugate gamma prior distribution such as OREDA (Offshore Reliability Data) and Poisson likelihood distribution. If there is no prior information, Jeffreys noninformative prior may be used. The LNG plant failure database was used as plant specific information. The PFDs (Probability of Failure on Demand) of IPLs (Independent Protection Layers) were estimated with the conjugate beta prior such as EIReDA (European Industry Reliability Data Bank) and binomial distribution. In some cases, EIReDA did not provide failure data, so the newly developed Frequency-PFD conversion method was used instead. By the combination of Bayesian estimation and LOPA procedures, the Bayesian-LOPA methodology was developed and was applied to an LNG terminal. The found risk values were compared to the tolerable risk criteria to make risk decisions and compared to each other to make a risk ranking. The Bayesian-LOPA methodology can be used in other industries. Furthermore, it can be used with other frequency assessment methods such as Fault Tree Analysis (FTA) and Event Tree Analysis (ETA) to strengthen their results. 

LNG (Liquefied Natural Gas) is one of the fastest growing energy sources in the U.S. to fulfill the increasing energy demands and diversify the energy portfolio. In order to meet the LNG demand, many LNG facilities including LNG importation terminals are operating currently. Moreover, there are many proposed projects for LNG terminals to fill the gap between supply and demand of LNG in North America. Therefore, it is important to control and estimate the potential risks in LNG terminals to ensure their safety and reliability.

Figure 1.   Description of an LNG importation terminal ( 

One of the most cost effective ways to estimate the risk is LOPA (Layer of Protection Analysis) because it can provide quantified risk results with less time and efforts than other methods. Thus, LOPA was applied in this research. For LOPA application, failure data are essential to compute risk frequencies (see Figure 2). However, the failure data from the industry are very sparse and have statistically shaky grounds due to insufficient population of sample data and relatively short-term operational history. Bayesian estimation is identified as one of the better methods to use to compensate for the weaknesses found in the LNG industry’s failure data. It can update the generic data with plant specific data. In other words, the data updated by Bayesian logic can reflect both long-term based historical experiences and plant specific conditions. Thus, in this research, the new Bayesian-LOPA methodology was developed as shown in Figure 3, and it was applied to an LNG importation terminal to estimate the potential risks.  

Based on Bayesian estimation, the frequencies of initiating events were obtained using a conjugate gamma distribution as the prior information and Poisson distribution as the likelihood function. OREDA (Offshore Reliability Data) database was used as a prior distribution because it was produced from a gamma distribution (see Figure 4). If there is no prior information, Jeffreys noninformative prior may be used. The LNG plant failure database was used as plant specific likelihood information. The PFDs (Probability of Failure on Demand) of IPLs (Independent Protection Layers) were estimated with the conjugate beta prior distribution and binomial likelihood distribution. EIReDA (European Industry Reliability Data Bank) database was used as prior information because it provided the failure data made from beta distribution. In some cases EIReDA did not provide failure data, so the newly developed Frequency-PFD conversion method was used instead. By the combination of Bayesian estimation and LOPA procedures, the Bayesian-LOPA methodology was developed. The method was applied to an LNG importation terminal. For seven incident scenarios, it produced valid risk values. The posterior values of every initiating event or IPLs are located between prior and likelihood values. This means that the posterior values are valid and well-updated.  The found risk values were compared to the tolerable risk criteria given by CCPS (Center for the Chemical Process Safety) to make risk decisions. Finally, the estimated risk values of seven incident scenarios were compared to each other to make a risk ranking in view of probabilistic risk analysis which considers only failure frequency without considering consequence analysis.  In conclusion, as the good safety records of LNG industries speak, in this research, it can be generally concluded that the LNG terminal has good safety protections to prevent dangerous events (see Figure 5). The newly developed Bayesian-LOPA methodology as one of the risk assessment methods really does work well in an LNG importation terminal and it can be applied in other industries including refineries, petrochemicals, nuclear plants, and aerospace industries. Moreover, it can be used with other frequency analysis methods such as Fault Tree Analysis (FTA) and Event Tree Analysis (ETA).

Figure 3.   The flow diagram of this research  

Special Thanks to :  
Geun Woong Yun
from Texas A&M University

How Is Lightning Made?

Wednesday, January 5, 2011

I live in Jogjakarta, Indonesia and almost everyday we see hard rain and lightning, here I will tell you about lightning.. 
Not this Lightning :)

But This is real LIGHTNING

How is lightning made? People used to make up stories to answer that question. Today, science tells us how.

You have heard of Ben Franklin. Did you know he flew a kite during a thunderstorm? He wanted to prove that lightning is a form of electricity. We know now that flying a kite in a storm is not safe. But, Ben was right. Lightning is a form of electricity. How does this "electricity" form?

What do You Need to Make Lightning?
You need cold air and warm air. When they meet, the warm air goes up. It makes thunderstorm clouds! The cold air has ice crystals. The warm air has water droplets. During the storm, the droplets and crystals bump together and move apart in the air. This rubbing makes static electrical charges in the clouds.

Just like a battery, these clouds have a "plus" end and a "minus" end. The plus, or positive, charges in the cloud are at the top. The minus, or negative, charges are at the bottom. When the charge at the bottom gets strong enough, the cloud lets out energy.

The energy goes through the air. It goes to a place that has the opposite charge. This lightning bolt of energy that is let out is called a leader stroke. It can go from the cloud to the ground. Or, a leader stroke can go from the cloud to another cloud. No one is sure why lightning bolts follow a zigzag path as they move. The main bolt or stroke will go back up to the cloud. It will make a flash of lightning. It will also heat the air. The air will spread quickly. It will make the sound we hear as thunder.

Be Safe in a Storm
Lightning is dangerous. Here are some safety rules.

  • Stay away from open spaces. But, do not stand under a tree. The best place is inside a building.
  • If you are swimming, get out of the water. Get out as soon as you see a storm coming. The storm may seem far away, but lightning can travel over 20 miles!
  • During a thunderstorm, shut off or unplug all electrical items. Do not use the phone.
  • Never walk in a thunderstorm carrying a metal pole. Don't even carry an umbrella!
  • How will you know if a lightning strike is near you? You will feel the hair on your head or body start to stand up. If this happens, go to a safe place. Go quickly! If there is no safe place near, get as close to the ground as you can. 
Scientists have learned some facts about lightning from pictures. Some lightning flashes are made up of as many as 25 or more lightning bolts (strokes). They move so fast that your eyes only see one flash!

Lightning is fun to watch. But, make sure you do so safely.  

Source :
Lightnign NASA Document
Lightning Wikipedia

Is not a problem when you try really hard but your ambition is not achieved yet. The problem is when in the middle of the road, you despair the opportunity from the Most Benevolent God's gives to achieve your ambition.

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