Monday, February 26, 2007

Risk management, anyone?

The secret of life? The secret's in the sauce.

- tagline of Fried Green Tomatoes (1991)

I'm excited. I'm just days away from employment in another - and far better - bank. I have one final interview left before finally saying goodbye to the unemployed sector of which I have been a desperate member for more than two months.

And the job? Risk management. Alright, it's the same job as Ben Stiller's in the movie Along Came Polly. Well, I just hope everythings goes well in my interview next week with the American group head for risk management in South East Asia who is based in Singapore.

Right now I'm reading about - guess what? - Financial Risk Management. Wikipedia really comes in handy, especially for totally ignoramus people like me. 

Friday, February 23, 2007

MRT moments

Pasahero 1: Padaan ho.
Pasahero 2: Wala nang lugar. Ang sikip sikip na!
Pasahero 1: Eh, galaw-galaw nang kunit para hindi ma-stroke!

*******

Pasahero1: Galaw ka naman dyan pare, ang sikip-sikip na dito.
Pasahero2: Gago ka pala eh, and sikip na nga!
Pasahero2: Eh gago ka rin!
Ako: (Silently) Mga gago pala tong dalawa...

*******

Pasahero 1: Ang sikip-sikip talaga sa MRT. Ang init!
Pasahero2: Di magtaxi ka na lang kung magrereklamo ka.
Pasahero3: Oo nga, magtaxi ka na lang!
Ako: (Silently) Ang sikip na nga, nakikisawsaw pa sa usapan 'tong isa dito...

Thursday, February 22, 2007

Unhappy Meals!



A Chicken McNugget is corn upon corn upon corn, beginning with corn-fed chicken all the way through the obscure food additives and the corn starch that holds it together.

-Michael Pollan, science journalist


I just finished reading an interesting article written by Michael Pollan and published in the New York Times about the prevailing dietary trends of Americans. Entitled Unhappy Meals, the article is fun to read as the author's wit and superb knowledge about the subject will never bore you as you go along the long essay.

You can read it here. It's quite long do, so take your time and grab your favorite vitamin fortified, low salt, low cholesterol, omega3-rich, and preservative-free chips -- and find yourself guilty of what Pollan calls Nutritionism.

Wednesday, February 21, 2007

the previous weeks

The previous weeks have been quite stressful for me. Not that I underwent extreme physical labor. What I experienced were more of disappointments and upturn of unexpected events that made my life more difficult and complicated, at least in this job hunting phase I'm in right now.

While in an interview in Ortigas:

"Is the company earning?" asked the General Manager of a multinational company who gave me a quantitative graph for analysis. I immediately said yes, noticing that the graph showed an increasing trend. That was the start of the booby which until now leaves me clueless as to why it happened to me.

It was as if a total black out closed down the entire circuitry of my brain. I was totally incapable of analysis, much less doing simple arithmetic operations. Imagine, I couldn't even arrive at the answer of - guess what - 5.3/1.06. It took me five minutes (or even more) to compute it. It was really a shame - a big shame on me. I spent four years in the university solving calculus problems and analyzing more complex graphs and just end up clueless as to how to determine simple ratios using arithmetic.

Later on when asked to explain the graph and still clueless, I went on stating the most stupid analysis I have ever made in my entire life. I watched in horror as my interviewee changed his facial expression, as if wondering if I ever am a UP graduate. Nevertheless, I got back on my senses towards the end of the interview and, to my consolation, I did answer correctly some of the questions. But it was too late already to undo what happened earlier. I went home wondering why it all happened. My important lesson: at least I learned that 5.3/1.06 is equal to 5!

During the PAASE international scientific conference in Century Park Hotel:

Being chosen as one of the presentors, I was supposed to speak about my undergraduate thesis. Hours before my presentation, GMA dropped by to deliver her keynote address to the scientific community whom she impressed with promises and financial support (well I do hope that at least half of them will be realized). She also took lunch there. Upon leaving, I was one of those who shook her hands (talk about being shtar shtruck! Hehehe).

When it was my turn to present, I was really very nervous. I thought that a three-day preparation was not enough, especially that I was going to talk in front of scientists from here and abroad. But thank God, everything went well. During the Q&A portion, the question asked by Dr. Baldomero Olivera (who, by the way, is this year's Harvard Scientist Awardee) was the one I expected the most: What is semidominant mutation? Thus, I gave the perfect answer (modesty aside, ahemm).

But the thing is that because of my trying too look and speak excellently in the conference, I’m now offered a job by Dr. Olivera and Dr. Concepcion in the Marine Science Institute of UP Diliman. They wanted me to join their group on their research on Conus and Turrid snails. Undoubtedly, these creatures are among the very amazing invertebrates on earth. They are very venomous (and many people don’t know about this) and live all throughout the archipelago (shallow or deep sea water). There have been reported incidents of people dying or injured because of these snails. More importantly, these snails hold a lot of promise for drug discovery – their venom is rich with a plethora of pharmacologically active peptides.

Surely, research work is very noble, intellectual, and, in the Philippine setting, very patriotic. However, I can’t see myself doing it. Though I finished molecular biology, I am now more inclined to pursue a career in the corporate world. And honestly, finding one is very difficult provided my background in science and my lack of technical knowledge in accounting and business. But I’m really trying hard to get a good job. Hopefully I’ll start working again in two weeks’ time.

Hence, I might not accept the job offer though I admire the efforts of Filipino scientists to advance science and research in the country amidst tremendous challenges. Indeed, what the Philippines needs is a robust scientific and research background to make it competitive. Yet, Filipino scientists and researchers, in spite their international fame and significant contribution to science, remain the most underpaid professionals in the country. How I look with utmost respect many scientists I meet in UP, but can’t resist feeling sorry over how their intellectual value is deemed insignificant by a society too preoccupied with other concerns, valid or not. They should also be called bagong bayani. I hope the government and the Filipino people will realize this soon, lest more and more Filipino talent, ingenuity, resource, and opportunity to excel in the international arena will be lost.

Presently:

Today is Ash Wednesday so I already heard Mass this morning. Earlier this morning I was observing the bird couple nesting in our garden. They're now teaching their fledglings how to fly! I’m now on my way to an interview in Makati in a company involved in mass media. Wish me luck!

Tuesday, February 13, 2007

IDENTIFICATION OF A TRUNCATING MUTATION IN THE HOMEODOMAIN (HD) OF PAX3 IN THREE GENERATIONS OF A FILIPINO FAMILY WITH WAARDENBURG SYNDROME TYPE 1

Part of a scientist's duty is to inform people - in layman's terms -
scientific breakthroughs that are relevant to society and to each one.
Thus, while preparing for an oral presentation this week for an international
scientific and engineering conference (PAASE), I thought it's good to post
the abstract of my undergraduate thesis.

Enjoy reading!

**********

IDENTIFICATION OF A TRUNCATING MUTATION IN THE HOMEODOMAIN (HD)
OF PAX3 IN THREE GENERATIONS OF A FILIPINO FAMILY
WITH WAARDENBURG SYNDROME TYPE 1

Andrew Agunod, Jr. and Cynthia Palmes-Saloma, Ph.D.
Laboratory of Molecular and Cell Biology, National Institute of Molecular Biology and Biotechnology
University of the Philippines Diliman, Quezon City

ABSTRACT

Waardenburg Syndrome is a rare autosomal dominant genetic disease characterized by defects of neural crest (NC) origin arising from mutations in genes associated with NC cell migration, differentiation, and survival during embryogenesis. We present three generations of a Filipino family with eight (8) Waardenburg Syndrome type 1 (WS1) affected members showing congenital unilateral or bilateral hearing loss, eye pigmentation defects, patchy hypopigmentation of the skin, white forelock, and dystopia canthorum. Mutations in the PAX3 gene which encodes a trancsription factor have been implicated in WS1. In this study, we screened for mutations in the DNA-binding paired domain (PD) and homoeodomain (HD) of Pax3 in all affected members. The paired domain which is frequently involved in WS1 cases and is encoded by exons 2 and 3 contained no mutations. However, in all affected members, there was a C→T transition in nucleic acid 1033 (C1033T) resulting to a nonsense mutation in codon 233 (R223X) affecting the homeodomain region, thus indicating that a mutation in one of the alleles of PAX3 is sufficient to cause the repertoire of neural crest abnormalities in WS1-affected individuals.

INTRODUCTION

Waardenburg Syndrome (WS) is an autosomal dominant neural crest abnormality associated with most common cases of congenital deafness. It has an incidence rate of 1 in 40,000 individuals and is known to exhibit wide genetic and clinical heterogeneity [1]. One of the four types of the disease is Waardenburg Syndrome 1 (WS1) which is characterized by dystopia canthorum (lateral displacement of the inner canthi of the eyes), congenital unilateral or bilateral sensorineural deafness, heterochromia irides (defect in eye pigmentation), white forelock, and patchy hypopigmentation of the skin.

The only causative gene associated with WS1 is the PAX-3 gene, coding for a transcription factor expressed by developing cells during embryogenesis. The neural crest cells that originate from the dorsal region of the neural tube actively express Pax3 which is required for their survival and differentiation into various tissues including the neurons in the peripheral nervous system, ganglia in the gut, pigment cells in the skin and eyes, and facial cartilage. PAX-3 is a member of the paired type gene family conserved among different species. It contains a paired box domain, an octapeptide, a homeodomain, and a Ser-Thre-Pro-rich COOH terminus. The paired box domain and homeodomain are conserved regions that bind to DNA and are essential for proper functioning of the Pax3 transcription factor which directly activates, in synergy with Sox10, the MITF gene that encodes another transcription factor critically involved in melanocyte differentiation through its action on tyrosinase gene expression [2]. Mutations in the Splotch locus of chromosome 1 in mice generate an animal model for WS1.

Sequence analysis of more than 90% of individuals with WS1 showed mutations in the PAX3 gene varying from simple single point mutations to large deletions. Mutations are numerous in the conserved regions of the paired box and homeobox regions found in exons 2-4 and 5-6 respectively. Knowledge on how these mutations caused the phenotypic characteristics seen in WS1 as well as the epistatic relationship between MITF and PAX3 have provided new insights on the role of genetic factors in the emergence of a disease phenotype that could help in the prognosis and management of the disorder.

In this study, we show that WS1 in three generations of a Filipino family is due to a C → Ttransition mutation in nucleic acid 1033 (C1033T) in the homeodomain region of one of the alleles of PAX3 resulting to a stop codon TGA in amino acid 233 of the transcription factor.

METHODOLOGY

Identification of a WS1 family. A three generation family with WS1-affected members was diagnosed by physicians studying pigmentary defects and was referred to us for further genetic workup. Affected individuals exhibited dystopia canthourm, a defining feature for WS1. Blood samples were collected from eight (8) available members of the WS1 family. A written consent was signed by the family members granting the researchers permission to use pertinent data and photographs for research publication purposes.

Genotyping and sequence analysis. Total genomic DNA was extracted from whole blood using Wang’s method. Primers were designed to amplify exons 2, 3 and 4, coding for the paired box, and exons 5 and 6 for the homeodomain of Pax3. Primers were designed to anneal at the intron-exon boundaries. Large scale PCR amplification was performed and the resulting products were gel-purified using Wizard® Minicolumn (Promega). Direct DNA sequencing using ABI-PRISM™ 377 DNA sequencer was then performed for all the samples. Sequences obtained were analyzed using Chromas™, Sequencher™ version 4.0.5 (Gene Codes Corporation, Ann Arbor, Michigan, USA) and Multalin™ (Corpet, 1988; http://prodes.toulouse.inra.fr/multalin/multalin.html). The PAX3 reference sequence was obtained from the Ensembl (www.ensembl.org) database.

RESULTS and DISCUSSION

Waardenburg Syndrome Type 1 is a genetic disease characterized by defects in neural crest cells during embryogenesis and has an occurrence of 1 in 40,000 individuals worldwide [3]. The pedigree of the three-generation family in this study exhibits an autosomal dominant mode of inheritance, confirming early investigations. There are 8 WS1-affected members in the family. The proband (II-5) has an affected father (II-1) and 3 of her siblings (II-1, II-10, and II-12), including herself, are also affected. Two (2) out of her 4 children (III-4 and III-6) inherited the disease while all the children of her normal siblings did not show any signs of WS1 (Figure 1 A). This pattern of inheritance where 50% of the children of an affected parent inherits the disease is characteristic of an autosomal dominant disorder.

Waardenburg syndrome is known to exhibit wide clinical heterogeneity due to differences in disease penetrance [1]. Affected members shows variable degrees of skin hypopigmentation, hearing loss, and eye and hair pigmentation abnormalities (Figure 1B). All were diagnosed with dystopia canthorum which is the defining feature for WS1. The full blown WS1 phenotype was observed in the sister and daughter (middle photo, Fig 1B) of the proband, who are both deaf-mute due to profound bilateral deafness, and have blue eyes and distinctive white forelocks. These symptoms were completely absent in normal members. The phenomenon of WS1 disease penetrance remains highly unclear. Moreover, while it was observed that some individuals with the same PAX3 mutation have varied phenotypes, there are those with a single base mutation and whole gene deletion that have similar features [4]. Nevertheless, genetic background and nonrandom environmental factors are pointed out to influence disease etiology [5].

The paired domain region is a critical binding domain of PAX3. Since the paired domain is upstream of the homeodomain, an abrogation at exon 2, 3 or 4 can lead to the abrogation of the homeodomain as well. Though mutations are numerous in both areas, mutations in the paired domain seemed more critical and more frequent in studies of WS1 families. PCR amplification of exons 2, 3 and 4 from the proband yielded fragments of 330, 312 and 382 bps, respectively. Products from exons 2 and 3 were gel-purified and sequenced. DNA sequences were visualized and edited using Chromas™ and sequence alignment was performed using Multalin™. The two exons subjected to direct sequencing revealed clean chromatograms with no indication of any sequence variations from the control. This result indicates that the paired domain of the proband is unaffected and suggests the existence of mutation(s) in some other part of the gene.

Primers FP and RP designed to amplify exon 5 showed products 240 bp in size. Products of the same size and intensity were amplified for all samples (Fig. 2A), eliminating the possibility of a large-scale deletion in the gene. Direct sequencing of Pax3 exon 5 DNA from the proband revealed a double peak for C and T as shown in Fig. 2B. The wild type C is located at nucleic acid 1033 and is part of codon 233 coding for arginine. Substitution by a mutant T (C1033T) in the sequence results to a stop codon (R223X) truncating the protein. PCR products were also sequenced indirectly by cloning in TOPO® vector. Sequencing revealed two alleles: a wild-type exon 5 with a C at nucleic acid 1033, and a mutant allele with a T at the same location (Fig. 2C). The same non-sense mutation was first described by Baldwin et al. [4] and is documented in the Human Gene Mutation Database (HGMD CM984205 www.hgmd.cf.ac.uk) as one of the causative mutations of WS1. This truncating mutation is detrimental to the proper functioning of Pax3 as it produces a protein without a DNA-binding homeodomain. Fortin et al [6] showed that the paired domain and homeodomain regions of Pax3, though individually possessing different sequence preference and high affinity as modular units, function interdependently and cooperatively in binding DNA in vivo. This implies that a mutation in either domain can lead to an impaired or dysfunctional transcription factor.

Direct sequencing of samples from other members of the family showed the presence of the same transition mutation C1003T in all WS1 individuals. The father, sister, son2, and daughter are heterozygous at the same region in the chromatogram while the unaffected husband, son1, and son3 demonstrated normal peaks (Fig. 3). This showed that the heterozygous allele C1033T was inherited by the proband from the father and was passed on to the third generation of her family.

One of the known functions of Pax3 is to transactivate the expression of MITF which is known as the master gene for melanogenesis (OMIM 156845). An impaired Pax3 affects the development of neural crest cell-derived melanocytes due to deficient levels of expression of the MITF gene that codes for a transcription factor which directs the expression of genes indispensable for melanocyte development such as the tyrosinase gene, TRP1, and TRP2 [2]. Melanocytes are responsible for pigmentation in the skin, eyes, and hair. They also form part of the cochlea of the inner ear. This explains the disease phenotype of WS1 patients where patients suffer from pigmentary anomalies in the skin, hair, and eyes and partial or bilateral hearing loss. Dystopia canthorum is present in almost all cases of WS1 and is considered as the defining feature for the genetic disorder. The phenotype is a direct consequence of mutations in Pax3 which is involved in the proper formation of facial structures.

In mice, a homozygous mutation in PAX3 is embryonic lethal due to an impaired development of the central nervous system. In humans, heterozygous PAX3 mutations lead to WS3, a more severe type with limb abnormalities. In another study, Pax3 was revealed to act in synergy with Sox10 in transactivating MITF expression [7].This provided an explanation for the molecular basis of WS4, another WS variant with additional feature similar to Hirschsprung Disease, implicating SOX10.

Primers designed to amplify the paired and homeodomains have been demonstrated to successfully amplify the desired regions from both wildtype and affected individuals. These primers can be excellent tools for screening for mutations in the Pax3 gene of WS1 patients.

CONCLUSION

Waardenbrug Syndrome Type 1 (WS1), a rare autosomal dominant disease, is known to be caused by mutations in the PAX3 gene. Pax3, a transcription factor, important for the development of neural crest cells, contains two DNA binding domains, namely the paired box and the homeodomain. Mutations in both regions have been known to cause WS1. The WS1 phenotype was observed in a three-generation family exhibiting defects in neural crest cell development such as eye pigmentation abnormality, skin hypopigmentation, whit forelock, dystopia canthorum, and sensorineural defects. Sequence analysis successfully established that exons 2 and 3 of the preoband was similar to the wildtype control. Direct and indirect sequencing of the homeodomain region of PAX3 revealed a heterozygous transition mutation in nucleic acid 1033 (C1033T) that resulted to a nonsense mutation R223X. This point mutation resulted to a truncated protein responsible for the characteristic WS1 phenotype in the three-generation family.

REFERENCES
(1) Waardenburg PJ. 1951. A new syndrome combining developmental anomalies of the eyelids, eyebrows and nose with pigmentary defects of the iris and head hair and with congenital deafness. Am Jorn of Hum Genetics 3:195-253.
(2) Bondurand N, Pingault v et al. 2000. Interaction among Sox10, Pax3, and MITF, three genes altered in Waardenburg syndrome. Hum Nolec genet. 9:1907-1917.
(3) Read AP and Newton VE. 1997. Waardenburg syndrome. J. Med. Genet. 34: 656-665. Retrieved March 21, 2006 from http://jmg.bmjjournals.com/cgi/content/abstract/34/8/656
(4) Baldwin C, Hoth C, Macina R and Milunsky A.1995. Mutations in PAX3 that cause Waardenburg syndrome type 1: ten new mutations and review of the literature. Am J of med genet 58:115-122.
(5) Morell R, Friedman, TB, Asher JH, Robbins LG. 1997. The incidence of deafness is non-randomly distributed among families segregating for Waardenburg Synsrome type 1 (WS1). J. Med. Genet 34:447-452.
(6) Fortin A, Underhill D and Gruss P. 1997. Reciprocal effectof Waardenburg syndrome mutations on DNA binding by the Pax 3 paired domain and homeodomain. Hum Molec Genet 6:1781-1790.
(7) Potterf SB, Furumura M, Dunn KJ, Arnheiter H, Pavan WJ. 2000. Transcription factor hierarchy in Waardenburg syndrome: regulation of MITF expression by SOX10 and PAX3. Hum. Genet. 107:1-6. Abstract retrieved March 20, 2006 from Pubmed database at http://www.pubmedcentral.nih.gov

Thursday, February 08, 2007

THE CALL

"Any intelligent fool can make things bigger, more complex, and more violent. It takes a touch of genius -- and a lot of courage -- to move in the opposite direction." -Albert Eistein

I was about to break down in utter hopelessness when suddenly a call came... Yes the call I have been expecting weeks before. I couldn't believe it, but that was the call, the call that would save me from the oceans of uncertainty.

Now what I have to do is to nurture optimism and get rid of this trifling pessimism that has clouded me for weeks. Andrew, wake up! You got a lot of things to do. Work! Work! Nunc!

Monday, February 05, 2007

JOBLESS BLUES I

Five months have passed since my graduation and I still linger on the nostalgia of my life as a student. Why? Simply because I still don’t know how it feels to be a professional. I still don’t have work!

My last months in the University were very tense: papers, thesis, org activities, and not to mention, a litany of exams which I have to go through before the UP grants me the diploma as passport to the professional world. I survived all of those and even graduated with honors – something which I became really proud of and gave me the impression that I was among the highly in demand graduates of the country. But I was wrong all the while!

Job offers didn’t arrive on a silver platter. My kayabangan, which by the way is typical to some students of the premiere state university, got the better of me when I didn’t start looking for a prospective job months before graduation. I held the impression that companies will compete against one another in hiring me once they know I’m from UP. But it seems that the State University no longer rings a bell. Until now, only a few of the companies I applied to responded.

But in fairness on my part and to my alma mater, my case is more circumstantial rather than due to my incompetence (here goes the kayabangan again). The one and only job I applied to last April was in the National Institutes of Health in UP Manila. I expected immediate hiring because I believed they would not have any doubts on me since I’m UP graduate myself. But UP, as any other government institutions, is a multi-layered bureaucracy. My first interview was on June, my second on July, and my appointment approval by the UP president is still unknown (even the personnel processing my documents are themselves uncertain of how long it will take). For one, applicants accepted last May aren’t yet working up to press time.

So on July I started to look for a job elsewhere and outside the course I finished. Molecular biology and biotechnology graduates in the Philippines (there are only around 30 graduates each year and only from UP) end up in the academe teaching or doing research, medical schools, or graduate schools abroad. Since I didn’t like to teach, didn’t have plans of studying again (still got to earn!), and no longer intend to go to med school (enough of headaches!), my only option was to do research. But pursuing such a career in a Third World country is not at all financially rewarding, not to mention the perpetual process of applying for the job (certificate of eligibility, medical exams, computer exams, two month-long interviews: by the time you start working, your first salary is not even enough to pay what you spent for all these!) Thus, I didn’t have any choice but to cross boundaries and see what’s in store for me in the corporate world.

Thanks to the internet, job seekers now have their best friends: jobstreet.com, jobsDB.com, and a lot other job websites seeking to help desperate job hunters in this country of around two million people unemployed (count me in!). These sites are where major companies (except for a select few) advertise their job vacancies and accept applications from job seekers who create and deposit their resumes online.

Through these websites I applied in top companies as Nestle, Unilever, Abbott Laboratories, San Miguel Corporation, Procter&Gamble, and so on. But I only received replies from a few companies because most of the job vacancies are in finance and marketing totally unrelated to my course in college, but not at all alien to me.

Since high school, business and economics have been among my interests along with science. But thanks to Discovery Channel and The National Geographic, my penchant for science – specifically molecular biology and medicine – flourished while my liking for anything that has to do with money drowned into the depths of today’s scientific revolution.

Have I got any regrets then? None at all! Molecular biology has been very exciting for me. I never thought that I will be doing the same stuff as the scientists I saw in TV when I was a kid. The DNA, immunology, cloning, molecular genetics, PCR, ELISA: only a privileged few – at least in a country like ours – are given the chance to learn these in lectures and experiments that often involve very expensive gadgets and reagents. I also had excellent company around; the best professors and the brightest blockmates (we have four summa cum laudes in the batch!). Taking the course taught me discipline in my studies and making good use of my time.

During these days, how much I long for the day when I start working. As each day passes, I get more and more desperate; but something inside tells me that the right job for me is coming. This leaves me thinking when that job is coming, and what a lot of stress it gives me!

*Written sometime August of last year. Watch out for Part II.

DILEMMAS AND DECISIONS



Call it a dilemma, the feeling as if the world is full of choices and yet you can’t decide. Call it a deadlock, the final moment when you have to decide but failed to do so. Call it a tragedy, a decision wrongly made. It is horrible.

Today’s world is an avenue of choices. Every stop is a matter decision. Every corner is another road that takes you to another route, another destination which you should take but failed to do so or should never but did so because you are not sure. You are lost. The world is full of possibilities, yet not all are good. For teenagers like me, these are realities which we have to face and live with everyday. Every moment of our lives is a matter of choice, and a wrong decision may mean a lot.

I remembered one summer when I was about 5 years old. In our province, like any other province in the country during hot seasons, rice paddies are dry. What were left in the fields were withered knee-high rice stalks on the scorched earth, making the plains an attractive and excellent playground for barrio kids like me. The dried paddies are perfect for kite flying, hide and seek, taya, and even for bullying around with my amigos. Playing under the sun during those days was like heaven for me, until one day I was not permitted by my mom to go out and play because of my asthma. My mom was not my problem though – for it was my aunt who was so strict.

One afternoon before sending me to sleep (I really hated sleeping during afternoons), my aunt told me to never set foot outside the house. I hesitantly said yes and forced myself to bed, knowing that she was sitting beside me and observing. After minutes of pretending to be asleep, I felt her left my side and heard her footsteps going upstairs. Alas! She went to her room to take a nap thinking I was already in dreamland. An opportunity came to me to escape to my ‘playground’, but that moment turned out to be a dilemma.

I was caught between obedience and the desire for fun. If I obey my aunt, I would be stuck in the house the entire afternoon in boredom; but if disobey, I would have fun the entire afternoon in the fields. I chose the latter. I did have a great time, but when I went home, I was severely punished. Imagine a child crying his lungs out, kneeling on salt. That was a lesson still vivid in my mind, and so was the horror of making a wrong decision.

During another summer when I was 10, a basketball clinic was held in our city. I haven’t yet learned playing basketball then, so I asked my mom if I could join – and she said no because I had asthma and I was fat. Helpless for she was never convinced, I obeyed. All my friends joined and learned how to play basketball very well. Until now, I still haven’t learned how to play the game. All I can do is dribble and shoot, and that’s all.

Looking back through these memories makes me realize that I was once punished for I disobeyed and lost an opportunity to learn for I obeyed. It compels me to think of how many decisions I have wrongly made and how much I have learned from them. It gives me fear thinking that I still have not learned; and now that I’m older, wrong decisions may spell disaster to my life.

Life now for me is more demanding and choices that I am faced with are more profound than whether to have fun or get bored alone. It is now more of whether you do what you ought to do or not. It is now more of a responsibility. Now obedience is no longer a matter of punishment and permissions, but a matter of will and generosity.

Now is the time when I have to make decisions that will change my life in a way that they will become my life. I have to decide on things fast and quickly, for my days are already counted before facing the ultimate end of everything. And when that very moment comes, I hope that I will never account to God for not living a life He wanted me to live.

As for my aunt, she now has her own family, happily living a life she willfully chose. And my mom, because of her love and self-giving, has taught me to give my best in whatever I aspire to do and in things I need to do – and it’s a whole lot better than learning basketball.

And now, it’s my turn to decide on important things – quickly and surely!

* Written on January 2004 at about 11 pm. The following day was a major exam and I was cramming. Thank God I still got a high mark.