New Study Shows Oxytocin Relieves Symptoms of Schizophrenia


Nasal  sprays containing the hormone oxytocin, nicknamed the “cuddle chemical” because it helps mothers bond with their babies, have helped people with schizophrenia.

Although the 15 participants used the sprays for three weeks only, most reported measurable improvements in their symptoms in this the first trial to test oxytocin in schizophrenia. “It’s proof of concept that there’s therapeutic potential here,” says David Feifel at the University of California in San Diego, head of the team running the trial.

Each participant received oxytocin or a placebo for three weeks, then the opposite treatment for three weeks with a week break in between.

On the basis of two standard tests for schizophrenia, taken before and after each block of treatment, participants averaged improvements of around 8 per cent when taking the oxytocin compared with the placebo (Biological Psychiatry, DOI: 10.1016/j.biopsych.2010.04.039).

The effects didn’t kick in until the final week, suggesting that it takes a while for the hormone to begin acting. “Standard antipsychotic drugs increase their efficacy several weeks later too, so oxytocin fits that profile,” says Feifel.

Feifel thinks that oxytocin is dampening down the excessive production of the neurotransmitter dopamine, which can trigger schizophrenic symptoms such as hallucinations. He says the rationale for treating people came from his own team’s studies showing that oxytocin could relieve a form of psychosis in mice, and research showing that people who sniffed nasal sprays of oxytocin became more trusting, which could ease paranoia symptoms in schizophrenia.

Feifel is seeking approval from the US National Institutes of Health for a larger trial testing oxytocin at a range of doses, and over a longer time.

“This work provides compelling data on the utility of oxytocin as a treatment for schizophrenia,” says Heather Caldwell of Kent State University in Ohio, co-author of a study in 2008 showing that “knockout” mice unable to make oxytocin were more prone to a form of psychosis.

By: Andy Coghlan / Courtesy: New Scientist

Role of Astrocytes In Generation of Sleep


If you’re feeling sleepy, it might be thanks to your astrocytes. This group of brain cells, long assumed to play a mere housekeeping role, may actually be responsible for controlling when we fall asleep, by releasing a chemical called adenosine.

“One of the leading theories of sleep generation comes from the observation that there is an accumulation of adenosine [in the brain] during waking, and that this adenosine decreases during subsequent sleep,” says Tommaso Fellin at the Italian Institute of Technology in Genoa. Adenosine is thought to suppress neurons which usually stimulate the cortex and keep it, and so us, awake. However, he says, “the cellular source of this adenosine has long been overlooked”.

Astrocytes play a key role in providing neurons with nutrients and aiding cell repair. In addition, unlike neurons that control immediate brain activity, astrocytes are thought to modulate longer-term activity by regulating communication between neurons. Because sleep pressure – the physiological mechanisms that result in the need to sleep – also builds up over a prolonged period of time, Fellin and Michael Halassa, now at the Massachusetts Institute of Technology, and colleagues, decided to investigate whether astrocytes might be the source of the adenosine that may drive the urge to sleep.

They used mice which had been genetically engineered to stop releasing adenosine from their astrocytes in response to an antibiotic in their food. Suppressing levels of adenosine reduced the length of sleep the mice took after being deprived of shut-eye for 6 hours, and prevented some of the cognitive defects associated with sleep loss (Neuron, DOI: 10.1016/j.neuron.2008.11.024).

“Our research suggests that these cells are responsible for adenosine accumulation” and the regulation of sleep, says Fellin, who presented the results at the Forum of European Neuroscience in Amsterdam, the Netherlands, last week.

“This is exactly the type of function that astrocytes would be expected to perform,” says Douglas Fields at the US National Institutes of Health in Bethesda, Maryland. “Astrocytes communicate slowly and on larger spatial scales than neurons. They are well suited to have a more global influence on brain function.”

By: Linda Geddes / Courtesy: New Scientist

The Biology of Fear


Any halfway decent thesaurus will provide a long list of synonyms for fear, and yet they are not very good substitutes. No one would confuse having the creeps with being terrified. It is strange that we have so many words for fear, when fear is such a unitary, primal feeling. Perhaps all those synonyms are just linguistic inventions. Perhaps, if we looked inside our brains, we would just find plain old fear.

That is certainly how things seemed in the early 1900s, when scientists began studying how we come to be scared of things. They built on Ivan Pavlov’s classic experiments on dogs, in which Pavlov would ring a bell before giving his dogs food. Eventually they learned to associate the bell with food and began to salivate in anticipation. Psychologists set up experiments to see if the same kind of learning could instill fear as well. The implicit assumption was that fear, like hunger, was a simple provoked response.

In one of the most famous (and infamous) of these experiments, American psychologist John Watson decided to see if he could teach an 11-month-old baby named Albert to become scared of arbitrary things. He presented Albert with a rat, and every time the baby reached out to touch it, Watson hit a steel bar with a hammer, producing a horrendous clang. After several rounds with the rat and the bar, Watson then brought out the rat on its own. “The instant the rat was shown, the baby began to cry,” Watson wrote in a 1920 report. “Almost instantly he turned sharply to the left, fell over on his left side, raised himself on all fours and began to crawl away so rapidly that he was caught with difficulty before reaching the edge of the table.”

The “little Albert” study, besides being cruel, was badly designed. Watson did not control it carefully to rule out a wide range of possible interpretations. In later decades, other scientists got much more rigorous in their study of fear, in many cases turning to rats rather than people as their test subjects. In a typical experiment, a rat was placed in a cage with a light. At first the light came on a few times so the animal could get accustomed to it. Later the scientists would turn on the light and then give the rats a little electric shock. After a few rounds, the rats would respond fearfully to the light, even if no shock came.

Further research revealed that the amygdala—an almond-shaped cluster of neurons deep within the brain—plays a pivotal role in the fear-association response in rats. Brain researchers discovered that the amygdala orchestrates human fear as well. The sight of a loaded gun, for example, triggers activity in this part of the brain. People with an injured amygdala have dampened emotional responses and so do not learn to fear new things through association. Science had identified a nexus of fear, it seemed.

Although this line of research yielded some major insights, it had an obvious shortcoming. In the real world, rats don’t spend their lives in cages waiting for lights to turn on; these experiments don’t capture the complex role that fear plays in a wild rat’s life.

In the 1980s Caroline and Robert Blanchard, working together at the University of Hawaii, carried out a pioneering study on the natural history of fear. They put wild rats in cages and then brought cats gradually closer to them. At each stage, they carefully observed how the rats reacted. The Blanchards found that the rats responded to each kind of threat with a distinct set of behaviors.

The first kind of behavior is a reaction to a potential threat, in which a predator isn’t visible but there is good reason to worry that it might be nearby. A rat might walk into a meadow that looks free of predators, for example, but that reeks of fresh cat urine. In such a case, a rat will generally explore the meadow cautiously, assessing the risk of staying there. A second, more concrete type of threat arises if a rat spots a cat at the other side of the meadow. The rat will freeze and then make a choice about what to do next. It may slink away, or it may remain immobile in hopes that the cat will eventually wander away without noticing it. Finally, the most active threat: The cat glances over, notices something, and walks toward the rat to investigate. At this point, the rat will flee if it has an escape route. If the cat gets close, the rat will choose either to fight or to run for its life.

Dean Mobbs, a neuroscientist at the Medical Research Council in Cambridge, England, wondered if humans have similarly layered fear responses. He and his colleagues were not about to send people into tiger-infested meadows, so they designed a clever alternative: They programmed a survival-themed video game that subjects could play while lying in an fMRI scanner. The game is similar to Pac-Man. You see yourself as a triangle in a maze and press keys to maneuver through it. At some point a circle appears. This is a virtual predator being guided by an artificial intelligence program to seek you out. If the predator captures you, you receive a small electric shock on the back of your hand.

This deceptively minimalist predator-prey game triggers some remarkably intense feelings. Mobbs measured the skin conductance of his players by rigging them up to a device similar to a lie detector. He found that when the predator was bearing down on players, they often experienced the same changes to their skin as those seen in people having panic attacks. Mobbs unleashed two kinds of predators on his players, a less adept one that was easy to escape, and a smarter one that was more likely to capture its victim. When people were chased by the better predator, they showed a stronger panic response in their skin, and they also crashed into the walls of the maze more often.

Meanwhile, striking changes were happening inside the brains of the players. The predators would first appear on the far side of the maze. While they remained at a distance, the same brain regions tended to become active in the players, a network that included parts of the amygdala as well as some other structures in the front of the brain. But when the predator was closing in, those brain regions shut down and a network of previously quiet regions farther back in the midbrain became active.

Mobbs’s results mesh nicely not only with the work of the Blanchards but also with some other, more recent studies of rat neurology. For example, one of the midbrain regions that Mobbs and his colleagues observed becoming active in humans when a “predator” was close is an area called the periaqueductal gray region. This area showed higher activity in the people who crashed into the walls more often, providing further evidence that it plays an important role in panic. Researchers have explored the anatomy of fear more directly in rats; by manipulating different areas of the rat brain, they are able to alter parts of the standard fear-driven sequence of behavior. When neuroscientists put electrodes into the periaqueductal gray region of rat brains and stimulated the neurons there, the creatures immediately started to run and jump uncontrollably.

Fear, the new results suggest, is not a single thing after all. Rather, it is a complex, ever-changing strategy mammal brains deploy in order to cope with danger. When a predator is off in the distance, its prey—whether rat or human—powers up a forebrain network. The network primes the body, raising the heartbeat and preparing it for fast action. At the same time, the forebrain network sharpens the brain’s attention to the outside world, evaluating threats, monitoring subtle changes, and running through possible responses. Another important job it performs is keeping the midbrain network shut down so that, instead of fleeing at top speed, a prey animal keeps very still at first. As the predator gets closer, however, the forebrain’s grip on the midbrain loosens. Now the midbrain becomes active, orchestrating a powerful, quick response: fight or flight. At the same time it shuts down the slower, more deliberative forebrain. This is no time for thinking.

It may be unsettling to find that our brains work so much like a rat’s. But the amygdala and the periaqueductal gray are ancient parts of the brain, dating back hundreds of millions of years. Our small hominid ancestors probably faced the same kinds of threats that baboons do today from leopards, eagles, and other predators. Even after we evolved the ability to use weapons and became predators ourselves, this ancient brain circuit still offered a useful defense against members of our own species.

Unfortunately, our exquisitely sophisticated brains may make this predator-defense circuit vulnerable to misfiring. Instead of monitoring just the threats right in front of us, we can also imagine threats that do not exist. Feeding this imagination into the early-warning system may lead to crippling chronic anxiety. In other cases, people may not be able to keep their periaqueductal gray and other midbrain regions under control. As we perceive predators getting closer, our brains normally make the switch from the forebrain to the midbrain regions. People who suffer panic disorders may misjudge threats, seeing them as far more imminent than they really are.

To test these possibilities, Mobbs and his colleagues are beginning to study people who suffer from fear-related disorders as they play the predator game. Such work may not uncover a biological distinction between angst and the heebie-jeebies, but it may show how much better we can understand ourselves—and tame our inner demons—once we appreciate the many dimensions of fear.

(By: Carl Zimmer,  Courtesy: Discover)

Life in Iran?


I am wondering how’s life in Iran following many reports that I’d read mentioning about smuggler, black market, sanction for Tehran’s nuclear program and the like.

The Independent reported 10 very surprising things about Iran.

1. Art-house Iranian films by such directors as Abbas Kiarostami and Mohsen Makhmalbaf wow foreign audiences.

2. Muslims are allowed to enter into temporary marriages with each other, sometimes lasting only a few hours. Critics say this in effect legalises prostitution, and women who enter into these sigheh contracts are often ostracised. But the practice is defended as a legal loophole to provide inheritance rights for children who would otherwise be born out of wedlock.

3. More than 3,600 Iranians have been killed in the past 25 years fighting heroin smugglers and the government has permitted radical measures to tackle the problem, including methadone programmes and syringe hand-outs to prevent the spread of disease.

4. Transsexuals are permitted to have sex-change operations in Iran by the decree of Ayatollah Ruhollah Khomeini.

5. According to the UNHCR, Iran hosts more than one million foreign refugees – more than any other country on earth. Most of these are Afghans and Iraqi Kurds, who fled their countries during the 1980s and ’90s.

6. While official dress codes are very strict, many young Iranians delight in pushing back the boundaries of what is acceptable. Teenage girls in Tehran wear the most vestigial of see-through headscarves and tight overcoats that barely cover the bottom.

7. Skiing is a major pastime in mountainous parts of Iran, but football remains the most popular sport.

8. Iran has one of the only condom factories in the Middle East, and actively encourages contraception as a means of family planning.

9. Satellite television is banned in Iran, but receiver dishes sit in plain view on top of many houses. The most popular channels are run by Iranians based in Los Angeles, who broadcast Iranian pop music and a steady stream of anti-regime propaganda

10. Iran is one of the world’s biggest producers of luxury foods.

Let me add few others:

1. It is one of the many paradoxes of the Islamic Republic of Iran that this most virulent anti-Israeli country supports by far the largest Jewish population of any Muslim country.

2. There is a Jewish representative in the Iranian parliament and there is a Jewish library with 20,000 titles, its reading room decorated with a photograph of the Ayatollah Khomeini.

Are Our Kids Creative?


Do you think Malaysian kids are creative?

Highly creative people tend to grow up in a families embodying opposites. Parents encourage uniqueness yet provided stability. They are highly responsive to to kid’s need yet challenged kids to develop skills. This resulted in adaptability, in time of anxiousness. In the space between anxiety and boredome was where the creativity flourished.

In childhood, distinct types of free play are associated with high creativity. Preschoolers who spend more time playing masak-masak or doktor-doktor have high measure of creativity. Playing someone’s else point of view helps develop their ability to analyze situation from different perspectives.

In middle childhood, kids create paracosms / fantasies of entire alternatives worlds. From then on school and studies become integral part of their world. Info become more complex and kids get overloaded and creativity suffers. (Write: Po Bronson & Ashley Merryman in Newsweek).

Malaysians have moved toward creativity. Check out at LimKokWeng’s University, KLIUC and ASWARA. Unfortunately, we started very late. Exposure in creativity should start in preschool years not when our youngsters start to join ASWARA. Because studies have shown that those high in creative self-efficacy had more confidence about their future and ability to succeed in life.

Aren’t that what we want?

The Switches That Can Turn Mental Illness On and Off


This story is about a tale of two rats. One rat got lots of attention from its mother when it was young; she licked its fur many times a day. The other rat had a different experience. Its mother hardly licked its fur at all. The two rats grew up and turned out to be very different. The neglected rat was easily startled by noises. It was reluctant to explore new places. When it experienced stress, it churned out lots of hormones. Meanwhile, the rat that had gotten more attention from its mother was not so easily startled, was more curious, and did not suffer surges of stress hormones.

The same basic tale has repeated itself hundreds of times in a number of labs. The experiences rats had when they were young altered their behavior as adults. We all intuit that this holds true for people, too, if you replace fur-licking with school, television, family troubles, and all the other experiences that children have. But there’s a major puzzle lurking underneath this seemingly obvious fact of life. Our brains develop according to a recipe encoded in our genes. Each of our brain cells contains the same set of genes we were born with and uses those genes to build proteins and other molecules throughout its life. The sequence of DNA in those genes is pretty much fixed. For experiences to produce long-term changes in how we behave, they must be somehow able to reach into our brains and alter how those genes work.

Neuroscientists are now mapping that mechanism. Our experiences don’t actually rewrite the genes in our brains, it seems, but they can do something almost as powerful. Glued to our DNA are thousands of molecules that shut some genes off and allow other genes to be active. Our experiences can physically rearrange the pattern of those switches and, in the process, change the way our brain cells work. This research has a truly exciting implication: It may be possible to rearrange that pattern ourselves and thereby relieve people of psychiatric disorders like severe anxiety and depression. In fact, scientists are already easing those symptoms in mice.

Two families of molecules perform that kind of genetic regulation. One family consists of methyl groups, molecular caps made of carbon and hydrogen. A string of methyl groups attached to a gene can prevent a cell from reading its DNA sequence. As a result, the cell can’t produce proteins or other molecules from that particular gene. The other family is made up of coiling proteins, molecules that wrap DNA into spools. By tightening the spools, these proteins can hide certain genes; by relaxing the spools, they can allow genes to become active.

Together the methyl groups and coiling proteins—what scientists call the epigenome—are essential for the brain to become a brain in the first place. An embryo starts out as a tiny clump of identical stem cells. As the cells divide, they all inherit the same genes but their epigenetic marks change. As division continues, the cells pass down not only their genes but their epigenetic marks on those genes. Each cell’s particular combination of active and silent genes helps determine what kind of tissue it will give rise to—liver, heart, brain, and so on. Epigenetic marks are remarkably durable, which is why you don’t wake up to find that your brain has started to turn into a pancreas.

Our experiences can rewrite the epigenetic code, however, and these experiences can start even before we’re born. In order to lay down the proper pattern of epigenetic marks, for example, embryos need to get the raw ingredients from their mothers. One crucial ingredient is a nutrient called folate, found in many foods. If mothers don’t get enough folate, their unborn children may lay down an impaired pattern of epigenetic marks that causes their genes to malfunction. These mistaken marks might lead to spina bifida, a disease in which the spinal column fails to form completely.

Other chemicals can interfere with epigenetic marks in embryos. Last year, Feng C. Zhou of Indiana University found that when pregnant lab rats consumed a lot of alcohol, the epigenetic marks on their embryos changed dramatically. As a result, genes in their brains switched on and off in an abnormal pattern. Zhou suspects that this rewriting of the epigenetic code is what causes the devastating symptoms of fetal alcohol syndrome, which is associated with low IQ and behavioral problems.

Even after birth the epigenetic marks in the brain can change. Over the past decade, Michael Meaney, a neurobiologist at McGill University, and his colleagues have been producing one of the most detailed studies of how experience can reprogram the brain’s genes. They are discovering the molecular basis for the tale of the two rats.

The differences between rats that got licked a lot and those that got licked only a little do not emerge from differences in their genes. Meaney found that out in an experiment involving newborn rat pups. He took pups whose mothers who didn’t lick much and placed them with foster mothers who licked a lot, and vice versa. The pups’ experience with their foster mothers—not the genes they inherited from their biological mothers—determined their personality as adults.

To figure out how licking had altered the rats, Meaney and his colleagues looked closely at the animals’ brains. They discovered major differences in the rats’ hippocampus, a part of the brain that helps organize memories. Neurons in the hippocampus regulate the response to stress hormones by making special receptors. When the receptors grab a hormone, the neurons respond by pumping out proteins that trigger a cascade of reactions. These reactions ripple through the brain and reach the adrenal glands, putting a brake on the production of stress hormones.

In order to make the hormone receptors, though, the hippocampus must first receive signals. Those signals switch on a series of genes, which finally cause neurons in the hippocampus to build the receptors. Meaney and his colleagues discovered something unusual in one of these genes, known as the glucocorticoid receptor gene: The stretch of DNA that serves as the switch for this gene was different in the rats that got a lot of licks, compared with the ones that did not. In the rats without much licking, the switch for the glucocorticoid receptor gene was capped by methyl groups, and the neurons in the underlicked rats did not produce as many receptors. The hippocampus neurons therefore were less sensitive to stress hormones and were less able to tamp down the animal’s stress response. As a result, the underlicked rats were permanently stressed out.

These studies hint at how experiences in youth can rewrite the epigenetic marks in our brains, altering our behavior as adults. Meaney and his colleagues cannot test this hypothesis by running similar experiments on humans, of course, but last year they published a study that came pretty close.

Meaney’s team examined 36 human brains taken from cadavers. Twelve of the brains came from people who had committed suicide and had a history of abuse as children. Another 12 had committed suicide without any such history. The final 12 had died of natural causes. The scientists zeroed in on the cells from the hippocampi of the cadavers, examining the switch for the stress hormone gene they had studied in rats. Meaney and his colleagues found that the brains of people who had experienced child abuse had relatively more methyl groups capping the switch, just as the researchers had seen in rats that had not been licked much as pups. And just as those rats produced fewer receptors for stress hormones, the neurons of the people who had suffered child abuse had fewer receptors as well.

Child abuse may leave a mark on its victims in much the same way that parental neglect affects rat pups. Abuse seems to have altered the epigenetic marks in their hippocampi. As a result, they made fewer stress receptors on their neurons, which left them unable to regulate their stress hormones, leading to a life of anxiety. That extra stress may have played a part in their committing suicide.

The hippocampus is probably not the only place where experiences rewrite epigenetic marks in the brain. An international group of researchers recently compared the brains of 44 people who had committed suicide with those of 33 people who died of natural causes. The scientists looked at a gene that produces the protein BDNF, which promotes hormone receptors, in a part of the brain called the Wernicke area. That area, located behind the left ear in most people, helps us interpret the meanings of words. In March the researchers reported that the BDNF switch had more methyl groups attached to it in the Wernicke area of suicide victims than in other people.

And the influence of environment doesn’t end with childhood. Recent work indicates that adult experiences can also rearrange epigenetic marks in the brain and thereby change our behavior. Depression, for example, may be in many ways an epigenetic disease. Several groups of scientists have mimicked human depression in mice by pitting the animals against each other. If a mouse loses a series of fights against dominant rivals, its personality shifts. It shies away from contact with other mice and moves around less. When the mice are given access to a machine that lets them administer cocaine to themselves, the defeated mice take more of it.

Eric Nestler, a neuroscientist at Mount Sinai School of Medicine in New York City, wondered what the brains of these depressed mice looked like. Last fall he reported discovering an important difference in a region of the brain called the nucleus accumbens. It was probably no coincidence that depression altered this region, since the nucleus accumbens plays an important role in the brain’s reward system, helping to set the value we put on things and the pleasure we get from them.

The change Nestler and his colleagues discovered in the nucleus accumbens was epigenetic: Some of the DNA in the neurons in that region became more tightly or less tightly wound in depressed mice. Such an epigenetic change might permanently alter which genes are active in the brains of those mice. The same may hold true for humans. Nestler’s team looked at cadaver brains from people who had been diagnosed with depression in life. They discovered the same epigenetic changes in the human nucleus accumbens.

If scientists can pinpoint the epigenetic changes that our experiences impart, it may be possible to reverse those changes. Nestler and his colleagues pumped drugs known as HDAC inhibitors into the nucleus accumbens of their depressed mice. These drugs can loosen tight spools of DNA, making it possible for cells to gain access to genes again. Ten days after treatment, the mice were more willing to approach other mice. The drug also erased many other symptoms of depression in the animals.

The possibility that we can rewrite the epigenetic code in our brains may be exciting, but it is also daunting. Modifying epigenetic markers is not easy—and that’s a good thing. After all, if our methyl groups and coiling proteins were constantly shifting, depression would be the least of our problems. Nothing ruins your day like finding that your brain has turned into a pancreas.

(By: Carl Zimmer, Courtesy: Discover)

Football Mania


Football and Parenting

Wow. The wife of WC final referee Howard Webb said she was amazed her husband was taking charge of the most important game in football given how he struggles to keep control of their children, Jack (son), Holly and Lucy (daughters).

Surely, taking charge of children isn’t similar to football. Football itself is a game. A family is totally not a game. It’s life full of dynamic, mystic and paradox at times. I like she uses struggle as life is a struggle with purpose. Football game is an hour and the half’s struggle but life is a struggle for the rest of your life.

How are we to compare football game and parenting?

Ironically, most parents think as some of them are good human resource managers, they shouldn’t have problem managing their kids. They would bring back all human resource theories that they had been practicing in their office just to find out that the theories are practically different.

Sure it is different. They should know by now why the employees and children are different…
_____________________________________________________________

Update:

This is taken from Newsweek (recent publication). Judge yourself.

The Link between Football and Jihad.

Osama BL is just one of the many jihadists who have used football to bring recruits into the fold. When he was in Sudan, it had its own league with regular practices and weekly matches between the squads. When Islamists flocked to Afghanistan to fight the Russians, Mujahiddin played mini WC on teams representing countries of origin. After the jihadists returned home, football was a way to keep in touch, particularly for Indonesians who formed the core of JI.

Indeed the link between football and militancy has been well documented as a ‘reliable indicator of whether or not someone joins the jihad’ as antropologist told a senate committee in March. Most of the participants in 2004 Madrid bombings played together [so what if they ate and played together? – ed]

One exception to this football mania. Somalia where militants have deemed the sport ‘ungodly’ and killed fans watching the WC.

It is Anger Control


How lucky for the seven Royal Malay Regiment privates for being sentenced to 7 years’ jail only after they pleaded guilty to causing the death of another private just because he was considered ‘lembik’ (feminine) after they assaulted him in a ragging incident in 2008.

I wonder whether 7 years jail would be OK for an attack which amounted to death. According to the case, the victim was hit on his private part using a rubber slingshot followed by another attack the next day which was characterized by punching, stepping on his body and back using spiked boot, hitting his head with a wooden item until the victim fell in the bathroom. And again this is because he was labelled as ‘lembik’. (STAR, July ,10). Can someone from the legal fraternity enlighten me on this?

Do they know who are their enemies and who are their friends? If they are too good in their job but there is nobody to kill, please send them to Gaza and let them fight with the Palestinian. If I am the judge that is what exactly I am going to do.

It is a shame when a judge’s husband was facing the same problem too. He pleaded guilty for punching a session court judge and was fine RM 2K under Section 323 of the Penal Code. The defense lawyer said: the incident was unfortunate as at that time, my client could not control his emotions.

Well said! Next time, all perpetrators with poor impulse control should be sent to Gaza for intervention by the Israelis. Let them learn the lesson.

Consumer Desire


Many people don’t know why it is important to understand the need of the consumer. That why when you go to the restaurant (except the mamak outlet), services are generally poor (except the 4- and 5-star restaurant). Orders are taken at their leisure, tables are not properly clean in time and even sometimes pay for the food creates a lot of hustle and difficulty.

What some ‘towkey’ of certain food outlets don’t really know is the psychology of consumer desire. Basically, people will act accordingly based on desire. Yes, for instance, if I am hungry (desire), I will act according to my desire of being hungry which could lead to getting easily irritable, angry and even avoid the unwelcoming restaurant altogether. The restaurant owner needs to fulfill this desire promptly so that it will be rewarding for customers and creates positive reinforcement when he/she will return to the outlet again.

To add more value to the owner advantage, he should serve products that connect well to the taste and imagination of the customers.

To my mind, that would explain why people like Dr Pauzi Abdul Majid like to entertain friends while watching World Cup in the mamak outlet. It’s psychology that matter. he..

p/s: Siapa menang World Cup, Pauzi?

Malaysia’s Plural Legal System


I was talking to the external examiner about the access to justice for Muslim women in Malaysia and noticed how superficial my knowledge are on Syariah law. Malaysia has a plural legal system that is contributed by the separation of Muslim customary and family law (Syariah law) to the common law.

All I can share with him is that in Malaysia there are differences in the legal treatment of family and matrimonial matters between Muslim and non Muslim. For Muslim, implementing Syariah law in toto is an obligation in the context of practicing Islam as the way of life. For non-Muslim, provision under Article 121 of the Federal Constitution gives an exclusive right for them to practice the secular matrimonial matters. Though both seen to be as zero sum game, when there is a conflict most judges will refer to the Federal Constitution of the country for reference.

Like it or not, there are some grey areas in relation to the relationship between Muslim and non-Muslim in case of divorce, the custody of children and the issue of one partner goes back to the original religion.

I believe I should read more on this as the subject matter and I would like to encourage my students to dwell further into these issues.