The Mind of the Mad Man

*A villanelle*

The mind of the mad man can see
where others don’t dare to dream.
The mind of the mad man is free.

Rules are made by the powers that be.
Though wiser than all they seem,
the mind of the mad man can see.

For salvation faith is the fee.
The sane get their light from a beam.
The mind of the mad man is free.

What we know of the world is a berry
in an infinite mass of cream.
The mind of the mad man can see.

A Book may be boat on a sea.
From the air, the sea is a stream.
The mind of the mad man is free.

They’ll lock him up and toss the key.
And although they ignore his scream,
the mind of the mad man can see.
The mind of the mad man is free.

Birth of the Whirlwind

*A Rondel*

Deep in the dark, a restless moth stirred.
The beetle beside him felt not a thing,
turned right around and slept like a king.
But all around the air had been angered.
It crossed the world, its particles clustered.
Wilder it grew from that flap of a wing.
Deep in the dark, a restless moth stirred.
The beetle beside him felt not a thing.

The wind escaped like a ghost from a cupboard.
It blew down a man who was a mountain climbing.
And aided another who had gone out sailing.
A whirlwind was coming and men spread the word.
Deep in the dark, a restless moth stirred.

Sestina to an Idealist

*For Crystal*

I gave you up for a night of passion.
That night shone bright. I thought that it was love.
The day came down, the night took flight. I live
and still I breathe but death is near I hope.
I tried to lie but though I tried, the truth
revealed. You left. I’m dying I believe.

I love you still, more than you know. Believe
me when I say, all the world of passion
means nothing without you. I hid truth.
I was afraid, you see. It’s hard this love,
for you have conquered me. I had no hope.
You stole my heart. It beat, began to live.

I favored dreams and death and could not live.
Fantasies were better, I did believe.
And then you came and I began to hope
that life awake was better. A passion
deep within my soul began to stir. Love
exposed my inner self. It betrayed the truth.

I longed to change the world for you, love. Truth
was, I knew not where to start, how to live
a life untainted by my dreams. My love
I thought was not enough. I now believe
what you had always known. Often passion
does not rage. It pulses, holds fast, like hope.

For you, my dear, had ever burning hope
that love prevailed. You always knew that truth
would someday burn apart, with passion,
all the shades that closed the mind. We would live
amongst the peasants and the king, believe
in things we’ve never seen, believe in Love.

I want that now. To live, to breathe, to love
to be alive. To dream, to do. To hope
although no one is hoping and still believe
through dying hope. To risk, to fight for truth.
And though I wish for death, I choose to live.
You spoke no words. I was lured by passion.

Your passion spoke like no word could.
I hope you know the truth. You saved me, I believe.
For you, O Love, you taught me how to live.

My Quest for Self in Fantasyland

I never knew it was called fantasy. I only knew that they were stories, and wasn’t all fiction a sort of fantasy anyway? By the time I discovered that those stories were part of a genre called fantasy, I was addicted. While I was the kind of reader who devoured everything with words on it—cereal boxes, signboards, fiction, non-fiction, you get the picture—reading fantasy, for me, was not just reading.

So why fantasy and not any other genre?

I recently pondered that question and realized that a lot of the fantasy that I had read and especially savoured were, in some way, stories of self-discovery. When I was younger, I used to wonder if I was real because I couldn’t see my own face. I didn’t know if I still existed when I wasn’t in front of a mirror.

But from fantasy and specifically, Neil Gaiman, I learnt that “things need not have happened to be true” and that I was real, even if I couldn’t see myself. Right now, I know who I am but while I sort of know who I am, the person that I know I am isn’t the person that I want to be.

This brings to mind Fat Charlie in Neil Gaiman’s Anansi Boys. At the beginning of the book, Fat Charlie is timid, easily embarrassed and although not married, already hen-pecked. He is stuck in a job he does not love, is not passionate about and has a boss whom he cannot stand up to. He starts off as a passive character. He doesn’t make things happen. Things happen to him.

What happens to him is the death of his father, Mr Nancy aka Anansi. Fat Charlie attends the funeral and finds out that his father has left him a whole lot of things, including a brother. His adventure really begins one night when, under the influence of alcohol, he talks to a spider on an impulse. His brother, Spider, shows up the next day.

Spider is the person that Fat Charlie has always wanted to be but could never muster enough courage to develop into. Spider is selfish, suave, confident and couldn’t care less about the world’s opinion of him. And like everyone who doesn’t care about the world’s opinion, he was loved or at least, treated with some sort of respect by everyone that he met.

The beginning of the turning point of the story is when Fat Charlie finally decides to do something. And even then, he makes this decision only because the situation presents itself to him. The singer at the restaurant at Saint Andrews happens to come to him and says, “What’s your name, darlin’?” (375)

She is asking him what his name is and Fat Charlie has the power to tell her. In fantasy, names are important, from The Amulet of Samarkand to Alice in Wonderland. Names are a sort of definition. Yvonne Bertills says in her study of proper and personal names that, “…a (personal) name is considered to be the essential linguistic label of individuals.” (17)

In The Lord of the Rings, one of Aragorn’s full names is Aragorn son of Arathorn. He is defined by where he came from, that is, his sire. Gimli is called the dwarf and Legolas, the elf. They are defined by their race. In the movie Beowulf, Unferth is called kinslayer. He is defined by what he has achieved ie. the killing of his brothers. In C.S. Lewis’ Narnia, the children are given names like Edmund the Just, Susan the Fair, Lucy the Brave and High King Peter the Magnificent. They are defined by their characteristics, which could be intrinsic (eg. values) or extrinsic (physical appearance).

When the microphone is in Fat Charlie’s face, he says his name—Charlie Nancy—but his voice “caught and wavered” (375). This shows that he is still trapped in the name that his father gave him—Fat Charlie. However, he is in the process of breaking free because he does what he would never have dared to do in the past.

He gets up onto the stage and he sings and he decides to fake a proposal to Daisy in order to save her from Grahame. Up till then, everything he had done had been a reaction to something or someone. The change in him started happening when he chose to act instead of just react.

Later in the book, after a conversation with his father and he had put on his father’s green fedora, he met Dragon, who said to him, “…You look remarkably like dinner.” (409)

But now, Charlie does not take this opinion passively. He dares to challenge it. He said, “I’m Charlie Nancy.” (409) After that, he is no longer called Fat Charlie, not even by Gaiman.

At the end of the book, both he and Spider have each developed into “complete” beings. Charlie Nancy, who before, had suffered from stage-fright is now a singer. He is confident and suave and people love him. He found himself.

In a way, I am a lot like Fat Charlie. In fact, I think I might be worse. I am exceedingly shy. I agree with others to avoid confrontation, even though on the inside, I am disagreeing. I smile when what I really want to do, is laugh out loud. Like Fat Charlie, I know I have a whole other side. I just have to find her.

Simon Goldhill writes in his book Love, Sex and Tragedy: Why Classics Matters, “Without self-awareness, without self-understanding, there can only be a fragile grasp on the questions that matter.” (8)

I agree with him on that point but while he says that self-awareness comes from studying the classics, I found that I discovered more about myself from reading fantasy. Fantasy gives me ideas and makes me think—another way fantasy makes me realize that I am. “Cogito ergo sum,” said Rene Descartes. Or in English, I think, therefore I am.

And although names are important, I think that my self-identity has got to be more than just my name. Simon Goldhill wrote, “The tragedy [Bacchae] demonstrates…that if you think the answer to the question ‘who are you?’ can and should be answered with a name, a family, a role, then you haven’t begun to understand ‘what your life is, nor what you are doing, nor who you are’—as the god Dionysius taunts us all.” (8)

In Coraline by Neil Gaiman, Coraline meets a talking cat who tells her that cats don’t have names and then goes on to say, “Now, you people have names. That’s because you don’t know who you are. We know who we are, so we don’t need names.” (43)

Mike Ashley says, in his essay on Coraline in The Neil Gaiman Reader, that, “It is…about a quest for identity and understanding of the world…” (172) Gaiman, through the cat reminds me that self-identity is not just in a name. The “self” is just something that one must know.

Fantasy is filled with characters who must remember who they are. From Harry Potter who must remember that he was the boy who lived, to Simba in the Disney cartoon The Lion King, who must remember that he is the rightful king. Throughout these stories, the protagonist is constantly reminded that he must remember who he is. The Lion King goes as far as having Mufasa say to Simba from the clouds, “Remember who you are.”

So like Fat Charlie, like Coraline, I am trying to find myself. And I am trying to remember who I am.

Now that I’ve “grown up”, I am expected to read more “serious” genres. But I wonder, what could be more serious than the discovery of self? Realist genres and non-fiction tell me who I am or who I am supposed to be but fantasy tells me, “Find out for yourself.” So every time someone asks me what sort of books I read, I say, “Oh, all kinds, you know, fantasy.”

In the end, I guess the reason that I keep reading fantasy is because I love stories and most of the storytellers that I love best, write fantasy. Neil Gaiman’s stories inspire me to tell stories of my own and in telling my own stories, I come alive and I find a way to define myself in a way that society might not understand but makes perfect sense to me.

In the book, Mr Nancy aka Anansi says, “…the stories change the tellers. Because now the folk who never had any thought in their head…now they’re starting to dream about a whole new place to live…” (341)

Works Cited

Ashley, M. 2007, ‘Coraline—A Quest for Identity’, in D Schweitzer (ed.), The Neil Gaiman Reader, Wildside Press, USA.

Bertills, Y. 2003, Beyond Identification: Proper Names in Children’s Literature, Abo Akademi University Press, Finland.

Gaiman, N. 2005, Anansi Boys, Headline Book Publishing, London. Gaiman, N. 2004, Coraline, Harper Trophy, NY.

Goldhill, S. 2005, Love, Sex and Tragedy: Why Classics Matters, John Murray Publishers Ltd, London.

Other Works

Beowulf 2007, Screenplay by Neil Gaiman & Roger Avary, distributed by Paramount Pictures (USA), Warner Bros. (International), ImageMovers (Japan), Performance capture film.

Campbell, J. 1968, ‘The Call to Adventure’, [in] The Hero with a Thousand Faces 2nd ed., Princeton University Press, New Jersey.

Lewis, C.S. 2005, The Chronicles of Narnia: The Lion, the Witch and the Wardrobe, HarperCollins, NY.

Lion King, The 1993, Screenplay by Irene Mecchi, Linda Wolverton, & Jonathan Roberts, distributed by Walt Disney Pictures, Feature animation.

Tolkien, J.R.R. 1966, The Lord of the Rings, George Allen & Unwin Ltd, Great Britain.

The modulation of apoptosis by Mycobacterium tuberculosis, how this affects the interaction between the pathogen and its host and the implications this knowledge has on the potential treatment of the disease

Abstract

Tuberculosis is a disease that is increasing worldwide and the drugs existent for vaccination and treatment of the disease are ineffective. The modulation of apoptosis by Mycobacterium tuberculosis, the microorganism that causes the disease, affects the pathogenesis of the disease. It occurs via a TNF-a-dependent pathway. Further understanding of the mechanisms involved and the interaction between the microorganism and the host could lead to development of drugs for vaccination and treatments.
Keywords: Mycobacterium tuberculosis, pathogenesis, apoptosis, drug development

Introduction

Tuberculosis is a wide spread disease and is a problem that is still increasing worldwide. This can be confirmed by WHO reports. There are vaccines against this disease—the one used most often is the Bacillus Calmette-Guerin (BCG)—but they are either only partially effective or are still in clinical trials. This situation is also encountered when treatment drugs are considered (Reece & Kaufmann 2008).

Tuberculosis is contracted when an individual inhales the bacteria Mycobacterium tuberculosis (M. tuberculosis). The bacteria deposits in the lungs and interacts with the cells there through various receptors. An immune response is triggered and a granuloma is formed. A granuloma is a nodule containing cells involved in the immune response and various other substances (Rock et al. 2008). These granulomas are mainly where apoptotic cells are found during an M. tuberculosis infection (Gil et al. 2002).

Apoptosis is programmed cell death activated by internal components of the cell. It is a natural occurring process in humans, with functions in embryogenesis, normal cell turnover and maintenance of the immune system. It is a more preferable option of cell death in these situations compared to necrosis, which is a passive death process and generally accidental, because it minimizes the damage to the other cells around the apoptotic cell (Lancelotti et al. 2006).

Apoptosis occurs as a defence mechanism against M. tuberculosis (Lee et al. 2006; Arcila et al. 2007) but some strains of the bacteria have developed methods of modulating this mechanism to their advantage (DeLeo 2004; Rajavelu & Das 2007).

Much research has been done on M. tuberculosis-modulated apoptosis because further knowledge on the mechanisms and genes involved could aid in the development of new drugs for treatment or vaccination (van Dixhoorn et al. 2008). Since apoptosis plays a key role in the pathogenesis of this disease, targeting the pathways involved in this process is a logical place to begin in drug development (Gil et al. 2003).

This literature review will outline the mechanisms involved in the M. tuberculosis-modulated apoptosis, the effects on the pathogenesis of the disease and touch briefly on the implications that further knowledge of this mechanism has on the development of treatments and vaccines.

Mechanisms involved in M. tuberculosis-induced apoptosis
`
Apoptosis can occur in response to bacterial infection (Lancelotti et al. 2006). This is an important part of the host defence system against M. tuberculosis (Arcila et al. 2007). The granulomas that contain the bacterial cells undergo apoptosis and the surrounding phagocytes engulf the remains of the bacterial and host cells (Rajavelu & Das 2007), effectively eliminating the bacterial cells.

In M. tuberculosis infections, apoptosis occurs in the infected cells by various pathways. The main pathway is a tumour necrosis factor alpha (TNF-a)-dependent pathway (Riendeau & Kornfeld 2003). TNF-a signals are released and it causes infected cells to undergo apoptosis. The signals are released in response to interactions between the bacteria and the host cells (Basu et al. 2007).

These interactions require receptors. Some of the receptors that have been found to play a role in apoptosis are the toll-like receptor (TLR)-2 and P2X7 purinergic receptors (Lopez et al. 2003; Placido et al. 2006). These receptors mediate the pathways for apoptosis of the host cells by being expressed in greater amounts in response to the presence of an infection (Placido et al. 2006). The genes coding for these receptors are activated in response to the presence of the bacteria (Rojas et al. 2002).

Other chemicals involved in signalling and regulation are nitrogen oxide and calcium. M. tuberculosis infections stimulate the production of TNF-a and IL-10. These control the production of nitrogen oxide, as well as activate caspase. Another pathway by which apoptosis is induced is the mitochondrial pathway. M. tuberculosis triggers a calcium influx and this causes the alteration of the mitochondria leading to apoptosis (Gil et al. 2002).

In other cases, the presence of specific receptors, such as TLR, in larger amounts than normal, causes the release of specific chemicals such as adenosine triphosphate (ATP), which is the major source of energy in the body, or enzymes that stimulate apoptosis. The general M. tuberculosis induced apoptosis pathway occurs via caspase pathways, that is, the enzyme caspase is required for apoptosis to occur. The type of caspase required varies between bacterial strains. In the event of an infection, a caspase cascade, that is, an increased flow of enzyme, occurs and this makes up part of the signalling during apoptosis (Rojas et al. 2002).

Other methods of signalling include release of interleukin (IL), cytokines and chemokines. These are all part of the immune system and sometimes result in an inflammatory response (van Dixhoorn et al. 2007).

In general, infection by M. tuberculosis results in apoptosis but there have been observations in which apoptosis did not occur. It was then suggested that there are strains of bacteria that are able to counter the host cell immune response. They do this by blocking part of the apoptosis pathway (Riendeau & Kornfeld 2003; Spira et al. 2003; Jayakumar et al. 2008). This is also a part of the modulation of apoptosis by M. tuberculosis.

Some strains of M. tuberculosis have proteins that interfere with the host signalling pathways such as protein kinase E (pknE). Bacteria with the gene coding for this protein are able to inhibit apoptosis (Jayakumar et al. 2008). Other strains down-regulate or decrease effectiveness of pro-apoptotic host genes (Spira et al. 2003), which means that some of the proteins that need to be synthesized in the host cell in order for apoptosis to occur are not synthesized.

Other bacteria have antigens that, when expressed, allows the bacteria to resist apoptosis (Mustafa et al. 2008). Although there are many different methods of resistance to apoptosis, the general idea is that the bacteria blocks a part of the pathway leading to apoptosis. A lot is still unknown about the mechanisms involved in the inhibition of apoptosis by M. tuberculosis.

Effects of modulation of apoptosis on the pathogenesis of M. tuberculosis

Even though apoptosis is part of the host immune system, modulation of apoptosis by M. tuberculosis plays a part in the survival of the bacteria (Sly et al. 2003; Jayakumar et al. 2008) and it is displayed in infections caused by virulent strains of M. tuberculosis. These strains of bacteria have stratagems to utilise the host immune system to their advantage (Spira et al. 2003).

Virulence, which is the degree of pathogenicity, is determined by the type of lipids found within their cell walls. Lipoarabinomannan and lipomannan are lipids found in the cell wall of M. tuberculosis and the ratio between them is what determines the virulence of the bacterial strain (Dao et al. 2004).

The virulent strains of the bacteria prevent apoptosis of the host cell and this provides a niche for their multiplication. The host cell acts as a secure environment so that multiplication of M. tuberculosis occurs at optimum rate (Sly et al. 2003). At the beginning of the infection, apoptosis is inhibited by the virulent bacterial strains because at this stage, apoptosis results in death of the bacterial cells (Sly et al. 2003; Placido et al. 2006).

Once the bacterial are stable and the growth of bacterial cells within the host cell is at its optimum, it induces apoptosis and causes lysis or destruction of the host cell. This allows the escape of the bacteria and the freedom to infect other healthy cells (Lee et al. 2006; Rajavelu & Das 2007). At this stage, the death of the host cell progresses very rapidly from apoptosis to necrosis (DeLeo 2004).

This sort of modulation of apoptosis by M. tuberculosis allows successful infection and spread of the disease tuberculosis. Much work has gone into the research of the pathways and mechanisms in order to determine which areas of the bacteria or the host would be the best drug targets.

Development of drugs and identification of drug targets

When considering the development of drugs, the target has to be identified. In tuberculosis, there is a high chance that the drug target is part of the apoptosis pathway because apoptosis plays an enormous role in the development of the disease (Lancellotti et al. 2006).

There are many other factors to be taken into consideration as well, such as the treatments required for different strains because each of these have different apoptotic pathways and different methods of pathogenesis. One example is the difference between the avirulent and virulent strains. The former induces apoptosis while the latter inhibits it (Sly et al. 2003; Lee et al. 2006).

One of the potential drug targets are the proteins involved in pathogenesis. Sly et al. carried out an experiment and found that virulent strains of M. tuberculosis prevented apoptosis by inducing an anti-apoptotic protein, Bcl-2, which is a member of the Mcl-1 family of proteins. Since apoptosis results in the death of M. tuberculosis cells, this process is a potential drug target. If the induction of the protein could be prevented, or the effect of the protein could be nullified, apoptosis would occur and result in death of M. tuberculosis (Sly et al. 2003).

Another protein involved in the inhibition of apoptosis is protein kinase E (pknE). M. tuberculosis without the gene coding for this protein, induced enhanced apoptosis while at the same time, inhibited necrosis. This protein is another potential drug target (Jayakumar et al. 2008).

Other potential drug targets would be the genes involved in regulation of apoptosis. For example, the gene coding for pknE. If the transcription or translation of the gene were prevented, apoptosis would still occur (Jayakumar et al. 2008).

Treatments also have to be administered at the appropriate times during the infection cycle. Treatments to induce apoptosis have to be administered in the earlier stages of infection because that is when apoptosis results in decreased viability of the bacteria (Spira et al. 2003; Placido et al. 2006).

After maturation of the bacterial cells, treatments that inhibit apoptosis have to be given so that further infection is prevented (DeLeo 2004). Other drug targets on the bacterial cell include antigens and the lipids within the bacterial cell wall (Mustafa et al. 2008; Rauwerda et al. 2008).

Another alternative is to target the host cells instead of the M. tuberculosis cells. Different levels of apoptosis occur in different types of cells. Apoptosis occurs more frequently in macrophages than in monocytes. Also, mature mononuclear phagocytes are more competent in containing the infection caused by M. tuberculosis compared to its immature precursors. Drugs that stimulate maturation of these cells can be used so that more mature cells are formed and the containment of the disease is possible (Arcila et al. 2007).

Receptors on the host cell can also be targets for drugs. The receptors could be altered so that they are resistant to inhibition by bacteria (Placido et al. 2006, Van Dixhoorn et al. 2003). Again, the time of the disease in which the treatment is administered has to be considered.

All these are potential targets of drugs and knowing the properties of these and understanding the mechanisms involved in the development of the disease could create new ways of regulating the development of the disease. Since both host cells and M. tuberculosis cells have a role to play in the progress of the disease, the drugs developed to treat the disease should focus on controlling the responses of both (Gil et al. 2002).

Conclusion

Tuberculosis is a disease caused by the bacteria M. tuberculosis. Host cells undergo apoptosis when faced with infection by this pathogen. This is part of the host immune response but some strains of this bacterium are able to counteract the host defense mechanism and use it to their advantage, which is, promoting their own survival. Various pathways are involved in the process of apoptosis and there are many proteins involved. Knowledge of how the pathways work and how the molecules involved interact with each other could result in the development of drugs and the identification of drug targets to be used in treatments or vaccinations.

References

Arcila, ML, Sanchez, MD, Ortiz, B, Barrera, LF, Garcia, LF, Rojas, M 2007, ‘Activation of apoptosis, but not necrosis, during Mycobacterium tuberculosis infection correlated with decreased bacterial growth: role of TNF-a, IL-10, caspases and phospholipase A2’, Cellular Immunology, vol. 249, pp. 80-93.
Basu, S, Pathak, SK, Banerjee, A, Pathak, S, Bhattacharyya, A, Yang, Z, Talarico, S, Kundu, M & Basu, J 2007, ‘Execution of macrophage apoptosis by PE_PGRS33 of Mycobaterium tuberculosis is mediated by toll-like receptor 2-dependant release of TNF-a’, Journal of Biological Chemistry, vol. 282, no.2, pp. 1039-1050.
Dao, DN, Kremer, L, Guerardel, Y, Molano, A, Jacobs, WRJ, Porcelli, SA & Briken, V 2004, ‘Mycobacterium tuberculosis lipomannan induces apoptosis and interleukin-12 production in macrophages’, Infection and Immunity, vol. 72, no. 4, pp. 2067-2074.
DeLeo, FR 2004, ‘Modulation of phagocyte apoptosis by bacterial pathogens’, Apoptosis, vol. 9, pp. 399-413. ®
Gil, D, Garcia, LF & Rojas, M 2002, ‘Modulation of macrophage apoptosis by antimycobacterial therapy: physiological role of apoptosis in the control of Mycobacterium tuberculosis’, Toxicology and Applied Pharmacology, vol. 190, pp. 111-119.
Jayakumar, D, Jacobs, WRJ & Narayanan, S 2008, ‘Protein kinase E of Mycobacterium tuberculosis has a role in the nitric oxide stress response and apoptosis in a human macrophage model of infection’ Cellular Microbiology, vol. 10, no. 2, pp. 365-374.
Lancellotti, M, Brocchi, M & da Silveira WD 2006, ‘Bacteria induced apoptosis: an approach to bacterial pathogenesis’, Brazillian Journal of Morphology, vol. 23, no. 1, pp. 75-86. ®
Lee, J, Remold, HG, Ieong, MH & Kornfeld, H 2006, ‘Macrophage apoptosis in response to high intracellular burden of Mycobacterium tuberculosis is mediated by a novel caspase-independent pathway’, The Journal of Immunology, vol. 176, pp. 4267-4274.
Mustafa, T, Wiker, HG, Morke, O & Sviland L 2008, ‘Differential expression of mycobacterial antigen MPT64, apoptosis and inflammatory markers in multinucleated giant cells and epitheloid cells in granulomas caused by Mycobacterium tuberculosis’, Virchows Archiv, vol. 452, pp. 449-456.
Placido, R, Auricchio, G, Falzoni, S, Battistini, L, Colizzi, V, Brunetti, E, Di Virgilio, F & Mancino, G 2006, ‘P2X7 purinergic receptors and extracellular ATP mediate apoptosis of human monocytes/macrophages infected with Mycobacterium tuberculosis reducing the intracellular bacterial viability’, Cellular Immunology, vol. 244, pp. 10-18.
Rajavelu, P & Das, SD 2007, ‘A correlation between phagocytosis and apoptosis in THP-1 cells infected with prevalent strains of Mycobacterium tuberculosis’, Microbiology and Immunology, vol. 51, no. 2, pp. 201-210.
Rauwerda, H, Breit, TM, Thallinger, GG & Wadee, AA 2008, ‘Gene expression profiling of suppressor mechanisms in tuberculosis’, Molecular Immunology, vol. 45, pp. 1573-1586.
Reece, ST & Kaufmann, HE 2008, ‘Rational design of vaccines against tuberculosis directed by basic immunology’, International Journal of Medical Microbiology, vol. 298, pp. 143-150. ®
Riendeau, Cj & Kornfeld H 2003, ‘THP-1 cell apoptosis in response to mycobacterial infection’, Infection and Immunity, vol. 71, no. 1, pp. 254-259.
Rock, RB, Olin, M, Baker, CA, Molitor, TW & Peterson, PK 2008, ‘Central nervous system tuberculosis: pathogenesis and clinical aspects’, Clinical Microbiology Reviews, vol. 21, no. 2, pp. 243-261. ®
Rojas, M, Olivier, M & Garcia, LF 2002, ‘Activation of JAK2/STAT1-a-dependent signalling events during Mycobacterium tuberculosis-induced macrophage apoptosis’, Cellular Immunology, vol. 217, pp. 58-66.
Sly, LM, Hingley-Wilson, SM, Reiner, NE & McMaster WR 2003, ‘Survival of Mycobacterium tuberculosis in host macrophages involves resistance to apoptosis dependent upon induction of antiapoptotic Bcl-2 family member Mcl-1’, The Journal of Immunology, vol. 170, pp. 430-437.
Spira, A, Carroll, JD, Liu, G, Aziz, Z, Shah, V, Kornfeld, H & Keane, J 2003, ‘Apoptosis genes in human alveolar macrophages infected with virulent of attenuated Mycobacterium tuberculosis’ American Journal of Cell and Molecular Biology, vol. 29, pp. 545-551.
Van Dixhoorn, MGAS, Munir, R, Sussman, G, Stad, R, de Haan, M, van der Hoeven, T,
Lopez, M, Sly, LM, Luu, Y, Young, D, Cooper, H & Reiner, NE 2003, ‘The 19-kDa Mycobacterium tuberculosis protein induces macrophage apoptosis through toll-like receptor-2’, The Journal of Immunology, vol. 170, pp. 2409-2416.

How I Was Wrong About Things, from Marriage to Black Pepper

The one thing I remembered clearly from that experience was the carpet burn on the small of my back. The redness lasted a week and the pain I felt every time my clothes touched the burn made sure I remembered. The other things slipped through my mind like things usually do. I could not remember what I was thinking or what we talked about. I could not even remember his name. I thought it might be Mark, or Adam or supercalifragilisticexpealidotious.

What can I say? He was a stranger, after all. That’s why I picked him. Here now, let me start from the beginning. Maybe then, this will all make sense.

I was twenty-one and I had never done it. In my circle, being a virgin was compulsory, that is, if you weren’t married. If you had no husband, or you had no wife, it was safe to assume that you were a virgin. It had something to do with staying pure and saving yourself for marriage.

Apparently, it was God’s law. And if you were a girl, it was man’s law that you stay a virgin until one of them came along and decided that you were pretty enough, smart enough, funny enough for them to want to enter into your inner sanctum.

I never believed in all that. I had decided never to get married so whatever sex I had would have to be with someone who was not my husband. The only reason that I had not had sex yet was because the right person had never come along.

My problem was that I disliked every boy that I knew. The chauvinist pigs disgusted me. I had no respect for the spineless, malleable ones. The charmers and the sissies irritated me. And on the top of that list were the stupid boys. The ones who never had a thought in their heads, who refused to listen to you, who thought they were always right and when they weren’t, ignored everything you said.

My brother said that I was jealous of them. Penis envy, he said. (He had been reading Freud.) He was wrong. I didn’t covet the penis. I coveted the freedom that the possession of a penis offered—to open doors, to blaze trails, to conquer the world. No one expected a boy to stay home, clean the house, cook, have children and change diapers.

The penis was like passport to be as obnoxious as you wanted, to be as loud and goofy and childish as you wanted. It was like a “Get Out of Jail Free” Monopoly card. If you had a penis, you got to have all the sex you wanted and your friends would pat you on the back and call you a stud. If you were a girl and you had all the sex you wanted, even your girl friends would avoid you and everyone called you a slut.

Somewhere in the West, way before I was born, someone fought for women’s rights. But what were they fighting for? Sure, I got an education. I even signed up to vote. I didn’t know what it was like in the West, but in the circle that I was in, a very Asian circle, I was still only just a girl. I would never be as important as a boy was. Even St. Paul said it—women stay silent in the church.

I had begun to give up hope of ever finding someone that deserved to “enter my inner sanctum”. I would have to hire someone, I thought. And then I thought, I should look for someone so absurdly good-looking that I could overlook all the other flaws. So when I found him, let’s call him Mark for now, I was relieved.

Mark had a superhero alter-ego sort of look, like he could appear in tights and a cape anytime and save the world. And above all, he was intelligent. I don’t mean that he got straight A’s in high school or that he knew everything there was to know in the world. When I say he was intelligent, I mean that he was capable of rational thought. After a brief conversation in a library (that was where we met), I knew that I had to have him.

It was the end of the year and I was about to graduate. Like I said before, I was twenty-one. I was studying abroad. I had wanted to stay at home where I knew my area, knew exactly where I was driving to and I could get all the kinds of food that I wanted. But my mother sent in the application forms and then put me on a plane.

Who knew what my mother was thinking when she coaxed me out of the country? Her friends’ children had gone and they never came home. Maybe she thought I would carve a life of my own somewhere else. But after a year in another country, I knew that even though life might be better or cleaner or safer, home was always the best place to be.

But at the time I met Mark, I was glad I was away from home. I could never have brought a strange man home, if I was living with my parents. And worse, I would never have been allowed to follow a strange man home, which was what I did. Come see my paintings, he said. Or maybe it was come see my library. I can’t remember.

Anyway, none of that matters. What matters is that I came to be in his house. I knew it was unsafe. He could have been a serial murderer but I didn’t care. I was twenty-one and I had never done anything significant in my life. The world would never notice if I disappeared off its face.

We walked around his house, I think. The only thing I remembered was his library. One whole room, devoted to books. I knew I had picked the right person—a book lover and a stranger. Erica Jong called it the “zipless fuck” in her book, Fear of Flying. The stranger the person was, the better. The less you knew of him, the easier it was to remove zips and buttons and hooks. It was so easy it was as if it was “zipless”.

Mark knew better than to offer coffee or tea or chocolate. Vodka? He said. I emptied one shot glass. All memory from then was a haze. The sharp press of the bookshelves, the taste of his tongue, the feel of something inside me, the soft roughness of the carpet, the books we looked at afterwards, the sound of our voices. All of them were dream-like when I tried to recall the experience later. It was a ritual, not an act of love.

Mark sent me home the next day and he lent me a book of poems. So I know I’ll see you again, he said. I still have that book of poems.

I waved goodbye and after he was out of sight, walked one block away to where I was actually living. My housemate was still in his pajamas. “Cereal?” he said when I walked in and then poured me a bowl just as he did every other ordinary morning.

I had always thought that I would feel a change within myself after I had had sex. I thought I would be more aware of the world around me. I thought everyone would be able to see something in my eyes and they would know that the word “virginal” no longer applied to me. But everything was still as normal as the day before and all I felt was fear. I could not remember if Mark and I had taken any precautions.

In erotica, they never have to worry about pregnancies or STDs or pain or feelings. Man and woman meet and they are instantly drawn to each other and they devour one another and then they orgasm simultaneously. Everything I had known about sex had been from books.

No one talked about sex. In my circle, if a girl talked about sex, the boys were either freaked out or immediately assumed that that girl wanted to get “down and dirty” with them. The strange thing was that both those categories of boys were classed under the same subset of “good Christian boys”.

I hated the Christian boys. They were self-righteous and uninformed and still believed that women should make leadership room for them. They could talk about sex all they wanted. With each other, that is. Girls should not even be thinking about having sex at all. Girls were prim, proper beings who had no sexuality.

The truth was that girls were as sexual as boys were. At least, I was. I had thought that I had known everything there was to know about sex. But just like my three-year Bachelor of Science course, I knew all the theory. I had had no practical experience.

I used to think that Forensic Science was exciting and glamorous. But after one semester of Forensic Chemistry experiments, I knew that the media was lying. With Mark, after all the kissing and the tingling, all there was, was a sharp pain. And then much later, the fear that I had not been careful enough.

The fear worsened when a month later there was still no bleeding. I had grey circles around my eyes during my graduation ceremony. When I sent my parents off at the airport after the ceremony, my mother made me promise to get enough sleep. I nodded because I couldn’t have told her that it wasn’t in my control. I simply could not sleep.

I was worried. I did not want a child. Children were noisy, dirty creatures. A baby would tie me down. And if it inherited anything from me, it would be a depressed neurotic, that did crazy impulsive things, like follow a stranger home and have sex and get pregnant.

But three home pregnancy tests later, with a week apart between each test, I knew the worst had happened. I had a parasite inside of me. I made an appointment at a clinic to get rid of it.

As fate would have it, I ran into Mark again (at the very same library). You never returned my book, he said. I shrugged and then I wondered if I should tell him about the thing and then I did. He oh-ed and then he wrinkled his brow and asked what I wanted to do about it. I shrugged, told him I was going to get rid of it. He offered to marry me. Who knew chivalry still existed? But I wasn’t a damsel in distress or a princess in her tower. I didn’t need to be rescued.

Besides, there was no way I could explain an impulsive marriage to my mother. Even worse, I would never be able to explain the thing that would come out of me in less than nine months afterwards. Church was a gossipy place. It was a shotgun marriage, the people my age would say. Then they would tell their mothers and those women would offer to pray for my mother. I could not put my mom through that kind of torture.

Or worse, behind my mother’s back they would say, “Such a bright girl, such a bright future and what good did her education do? She still got married right after graduation.”

I had often wondered about that. My mother’s friends had said to her, “Aiya, your daughter is just a girl. No need to study so high. She will get married what.”

So what? I wanted to yell at them. So what if I was going to get married? Why was it that a woman always had to choose between a career that she loved and the children that she loved? Why couldn’t a woman have both? A man could have children and a career. Why was it different for women?

So I said no to Mark. I said that I did not want an obligatory marriage. Mark pressed his lips together and his aura was forbidding but he nodded and said, okay then I’ll go with you. I thought I should have disagreed but I didn’t.
I remembered bits of our conversation from that night I spent at his house and I thought it might be nice to have him around. So I said he could come for the abortion and I told him when. I even gave him my number and told him where I really lived.

I know you think that this story will have a good, moral ending, where I change my mind and decide to raise the baby on my own and all that Hollywood crap. I didn’t. I had the abortion. Then Mark drove me home and I didn’t even shed a tear.

Until a month ago, that is. Almost two years had gone by but when my baby, Danny was born, I remembered that other child that I lost. I didn’t even know if it was male or female. I had managed to wipe most of that time out of my memory.

After I had packed up my life abroad, I came home. My family had missed me. My friends had organized reunions. It seemed that if I had really disappeared off the face of the world, people would have noticed.

I introduced my ang mo (Caucasian) boyfriend Christopher to all of them. Christopher and I got married soon after. I know I said I would never get married but that was before I knew that Christopher existed. I tended to dislike everything in general, from marriage to black pepper.

Christopher got a teaching job at a private school. I did what I would have done if Science hadn’t gotten in the way. I wrote plays and stories and essays about stories. I loved being married and I found out that black pepper went quite nice with beef.

Then, I got pregnant and everyone congratulated me. This time, I wanted the baby because if he were anything like Christopher, he would be caring and intelligent. I couldn’t wait for him to be born. But when Danny was born, my mother was the happiest person in the room. On that day, I remembered that other child, and for the first time, I cried for it.

Christopher knew exactly what I was crying about. He said I should write it down. Not for anyone to see or anything but just to let it out. To give that child that was lost some sort of immortality. So that I would remember. “Write it down,” Christopher said.

So I did.

Oh, and one more thing. That day at the library, when I had given Mark my number, he said, “In case you’ve forgotten, my name’s Christopher.”

*Check out more fiction at The Writer is a Liar.*