Nerdy Science Blog

Bernama (21/5/2008):

KUALA LUMPUR, May 21 (Bernama) — Dutch biotechnology company Ingrepro BV Wednesday announced its plan to invest over 10 million euros (RM49.8 million) in algae plantations for healthcare products, feed additives and development of the PowerFarm concept in Malaysia.

The PowerFarm to be set up at Technology Park Malaysia is an industrial large scale algae production plant to produce cradle-to-cradle renewable biodiesel and biogas.

It will produce algae for biomass using industrial and agricultural waste water, said Ingrepro’s director and chief executive officer Carel Callenbach after signing a technology transfer and business collaboration agreement with Biomac Corp Sdn Bhd and a memorandum of understanding with Algaechem Sdn Bhd here.

It’s good to hear that there are more biotechnology companies invest in Malaysia. Malaysia has stable and suitable weather conditions for growing algae. Algae can be used as fertilizer, alternative energy source (as mentioned in the news), pollution control (the use of wastewater), produce stabilizing substances, and nutritious (can be made into food, such as seaweed a.k.a. “fat choy“). Algae also can be used as agar, chemical dyes and coloring agents. Cosmetics products can also be made by using microalgae.

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The Age (22/5/2008):

AUSTRALIAN research giant the CSIRO has been forced to slash about 100 jobs and close two laboratories after large funding cuts in last week’s federal budget.

The announcement, made yesterday, will result in the closure of a horticultural research laboratory near Mildura, with the loss of up to 30 jobs, and a beef research laboratory at Rockhampton.  Some staff from the Victorian laboratory will be moved to Adelaide.

The move was denounced by the CSIRO Staff Association, which said work at the two laboratories contributed to Australia’s food quality and security.

The Federal Opposition was also scathing, with Senator Eric Abetz, accusing the Government of breaking a promise.  “Labor promised to revitalise the CSIRO, but have done the complete opposite,” he said.

The CSIRO’s budget was effectively cut by $63.4 million over four years.  Science and Research Minister Kim Carr said the Government had to take “tough decisions” in the budget as part of its “war on inflation”.

He described the CSIRO as “a great Australian institution” and said the Government had boosted its funding in areas such as researching “clean coal”, but difficult choices had to be made.

CSIRO chief executive Dr Geoff Garrett conceded the cuts would have an “adverse impact on research”, but said the organisation was moving funding away from “incremental research” in food production and supply.  Instead, the CSIRO would boost its investment in areas including energy, water and climate.

But the president of the CSIRO Staff Association, Dr Michael Borgas, said closing its laboratory at Merbein near Mildura would hurt the local horticultural industry.

Dr Borgas described the closures as “lazy, knee-jerk management” and attacked the budget cuts.

“If Australia is to meet the many challenges we face in relation to global warming, water and food security and quality, we should be boosting — not cutting — support for the CSIRO,” he said.

I feel bad for those 100 people who will lose their jobs.

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This is the evolution of apples!

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BERNAMA:

Malaysia Sees Potential In Tissue Banking

KUALA LUMPUR, May 20 (Bernama) — The development of the science of tissue banking in Malaysia will contribute substantially to the biotechnology sector as it could lower the cost for Malaysian patients in need of such care.

Datuk Iskandar Mizal Mahmood, chief executive officer of Malaysian Biotechnology Corporation (BiotechCorp), said today that for the development of tissue banking, Malaysia needs to industriously complement the efforts of the National Tissue Bank and Nuclear Malaysia in stepping up commercialisation of tissue banking.

The Tissue Engineering and Stem Cell Technology Report 2007 published by Visiongain estimates the market for future tissue engineered products, including regeneration of bone, cartilage and other connective structural treatments, at US$5 billion globally, he said.

“The market value of tissue banking could contribute to the Malaysian economy even though there are no definitive numbers as yet for Asia or the Asia Pacific, but the growth of the business in key markets in India and China is more than positive,” he said.

According to NovaSterilis, a US company which provides sterilisation technology for medical devices and human tissue, indicated that the US tissue bank market was worth US$400 million last year, he said.

“Tissue banking offers exciting possibilities in managing complex bone and cartilage diseases, spinal cord injuries and other serious injuries. It also prolongs life and adds meaningful years of freedom and mobility not only for the elderly but also for our children and youth by crippling diseases,” he told a press conference here on the forthcoming 5th World Congress on Tissue Banking.

Malaysia’s National Tissue Bank is recognised for producing safe, high quality tissue grafts in a wide field of application for burns, orthopaedic, microsurgery, facial, dental and paediatric surgery, according to Iskandar.

The National Tissue Bank’s research & development activities had achieved outstanding international work, with more than 40 research findings in amniotic membranes, bone grafts, trauma and reconstruction.

“Integrated research is also conducted in bio-materials, tissue engineering and stem cells,” he said.

Meanwhile Iskandar said that with the contribution of Nuclear Malaysia and other Malaysian participants, the 5th World Congress on Tissue Banking here on June 3-5 will feature speakers from 20 countries including the US, Cuba, UK, Germany, Belgium, Poland, Russia, India, Korea and Hong Kong.

– BERNAMA

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Based on my observations, most successful blogs (in term of having large amount of traffic) have great contents. “Content is king” is an old saying. What kind of contents that actually drive a blog to the peak? I categorized them into four types of posts and two classes. The two classes are long-term and short-term traffic posts. “Case history” and “tutorial” types are belonged to long-term traffic class, whereas the “issue” and “news” types are the short-term class.

1. Case history.

A timeless post that can be read anytime by anyone (people still quote Aristotle today). Case history type of posts can be successful story of a person, or the discovery and invention of a product, the application of certain knowledge.

Example: the myth of two-headed snake

2. Tutorial posts.

Tutorial posts also known as how-to posts. These posts teach readers new skills or knowledge. They also help readers to perform something better and solve their problems. Readers tend to bookmark this kind of posts and share with their friends. They will turn to you when they are in need.

Examples: How To Perform Plate Streaking, How To Make A Bouncy Egg

3. Issue posts

Being controversial is one of the ways that popularizes a blog. Writing current hot topical and controversial issues can peak your traffic in a short time, but such traffic also go as fast as it came. You can also interact with readers by asking questions, such as “should evolution be taught in school?” This can bring out the conversation and makes readers stick to your blog.

Examples: The PCR Song, The Job Perspective of Forensic Science Graduates in Malaysia

4. News.

A quick update of news in your niche fields also help to bring visitors to your blog. These readers might not have time to read through every piece of news, but their life become easier with your help to filter the news.

Examples: Finding of ManPig, The Helmet That Makes You Smart

Good contents make your blog become a good blog, but you need to market your blog to convert it to a great blog.

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Sometimes some group of people are extremist.  When there is gain, there is pain.

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I just got back my immunology essay today. I got distinction for this essay. I missed out some points, made a lot of grammatical mistakes, and also poor analysis and critical thoughts. I guess it’s better to copy and paste my assignments (after graded) as I don’t want to waste my time and efforts just to write it for the marker to read it once. Instead of keeping in my computer, I post it here for other students who might need a reference on this topic (please do not plagiarise).

Title: Cross-presentation of Antigens by MHC Class I Molecules

Introduction
Cross-presentation is important in immunological mechanism against tumours and viruses and it was first described by Bevan (Van Kaer, 2002; Bevan, 1976). It is the process of antigen-presenting cells (APCs), particularly dendritic cells (DCs), to capture extracellularly derived antigens (predominantly in the form of protein), process and cross-prime to CD8+ T cells (CTLs) via major histocompatibility complex (MHC) class I molecules (Guermonprez and Amigorena, 2005; Lizee et al., 2003; Shen and Rock, 2006). Many evidence showed that cross-presentation by APCs via MHC class I molecules were important to viral invasion. Many tests were conducted to understand the intracellular routes of cross-presentation in DCs. Further understanding of cross-presentation is also essential in designing better vaccine.

Importance of Cross-Presentation by MHC Class I molecules.
CTLs are important in antiviral immunity. The outcome of cross-presentation by MHC-I molecules can either be tolerization or priming of CTLs, which regulates and initiates immunity (Guermonprez and Amigorena, 2005; Fonteneau et al., 2003).

Most of the viruses do not have access to the routes for MHC-I cross-presentation to APCs due to the lack of specific virus receptor (Fonteneau et al., 2003; Freigang et al., 2003). This indicates that APCs present antigens acquired from other infected cells. APCs will then process these antigens in specialized pathway and load it onto MHC-I to cross-prime CTLs. Evidences showed that cross-presentations by DCs were the main mechanism that generated antiviral CTL-mediated immunity (Lizee et al., 2003). If there is any defection in cross-presentation elements, this can cause dysfunction of viral immune response. Mutagenesis in MHC class I cytoplasmic tail showed that transgenic mice could not respond to vesicular stomatitis virus (VSV) and Sendai virus (Lizee et al., 2003). Even if DCs were infected with vaccinia virus, they still can activate naïve CD8+ T cells in lymph node (Norbury et al., 2002). Cross-presentation does not only initiate antiviral immunity, but also important in maintenance of T cells tolerance to self-antigens (Fonteneau et al., 2003).

Intracellular Routes Involved In Cross-Presentation
Intracellular routes of cross-presentation had been studied extensively in DCs in vitro and in vivo. Figure 1 showed that there were five potential intracellular pathways being defined, which were vacuolar pathway, phagosome-to-cytosol-to-phagosome pathway, phagosome-to-cytosol pathway, GAP junction pathway, and retrograde pathway (Chen et al., 2008; Shen and Rock, 2006; Moron et al., 2004).

Figure 1. Potential mechanisms of cross-presentation (a) The vacuolar pathway. (b) Phagosome-to-cytosol-to-phagosome pathway. (c) Phagosome-to-cytosol pathway. (d) GAP junction pathway. (e) Retrograde pathway. (Shen and Rock, 2006)

Vacuolar pathway is transporter associated with antigen processing (TAP) independent and insensitive to proteasome inhibitors. Internalized antigens are degraded into peptides by cysteine protease cathepsin S in phagosome. Peptides are then loaded onto MHC-I. The resulting complexes are then transported to the cell surface through vesicular recycling (Chen et al., 2008; Shen and Rock, 2006). Cross-presentation in DC was blocked when protease inhibitor was used to inhibit cathepsin S activity in TAP-independent APC (Shen et al., 2004). Heat shock protein (HSP) enhanced murine macrophages which had their golgi inhibited by brefeldin A (BFA) showed that vacuolar pathway did not require ER and also TAP (Tobian et al., 2004). Inhibition of TAP in macrophages with US6 did not affect the rate of cross-presentation (Ackerman et al., 2005). Inhibition of proteasome did not block cross-presentation as well (Shen et al., 2004).

Cells have been known that they are electrically coupled through small channels. These small channels are called GAP junction, and they connect cytosols of adjacent cells. GAP junction allowed APCs to acquire peptides from other cells, and carried out cross-presentation. This pathway is called GAP junction pathway and it is TAP-dependant but proteasome-independent (Shen and Rock, 2006; Neijssen et al., 2005).

Phagosome-to-cytosol-to-phagosome pathway is proteasome- and TAP-dependent. MHC-I, TAP, Sec61 and other endoplasmic reticulum (ER) molecules are obtained by phagosomes by fusion with ER. Then the internalized antigen is exported to cytosol by Sec61 to the cytosol. The antigen will be degraded by proteasome and the peptides are transferred into phagosomes by TAP and bind with MHC-I (Shen and Rock, 2006). Sec61 also play a role in exporting internalized antigens to cytosol from ER and also introduce secretory or transmembrane polypeptides cotranslationally into ER (Ackerman and Cresswell, 2004).

Phagosome-to-cytosol pathway is proteasome- and TAP-dependent pathway. Exogenous antigens are internalized into phagosomes and transfer to cytosol. Proteasomes then degrade the antigens. The resulting peptides will be transport to MHC-I molecules in ER by TAP (Chen et al., 2008; Shen and Rock, 2006). Studies found that tyrosine-based endolysosomal targeting signal was important at sorting the MHC-I into vacuolar compartments (Lizee et al., 2003; Shen and Rock, 2006).

Retrograde pathway is proteasome- and TAP-dependent. Antigens are internalized into endosomes and retrograde into ER. Antigens will then be degraded by ER-associated proteasomal degradation (ERAD) in cytosol. Sec61 was found to involve in the retrotranslocation process (Ackerman et al., 2006). Its suggested functions were to move misfolded proteins into the cytosol for further degradation, and to remove unstable or accumulating proteins (Ackerman and Cresswell, 2004). Peptides are then transported back to ER and loaded onto MHC-I molecules by TAP (Chen et al., 2008; Shen and Rock, 2006). This model only cross-primes CD8+ T cells at high concentration in vitro and its importance is unclear (Shen and Rock, 2006). Endosome or macropinosome with ER membrane can also lead to wrong reasoning that ER is involved in this pathway (Ackerman et al., 2006).

Most of the routes also required proteasomes to degrade antigens to peptides. Proteasomes were found to degrade many antigens for easier loading onto MHC-I molecules (Fonteneau et al.¸2003). Different peptides are generated by different proteasomes (Ackerman and Cresswell, 2004). Tiwari et al. (2007) demonstrated that endosomal processing was important for generation of MHC-I binding peptides. Vacuolar proton pump was inhibited with pH neutralizing drugs with acidophilic amines, and the loading process of peptide to MHC-I was suppressed (Tiwari et al., 2007).

ER was essential to transport peptides loaded MHC-I molecules to the cell surface (Fonteneau et al., 2003; Brophy et al., 2007). When BFA was used to inhibit peptide transport through Golgi, the presentation of certain peptides on MHC-I was blocked, and TAP was not essential in presenting these peptides (Brophy et al., 2007). This indicated another potential intracellular route in cross-presentation. In contrast, Chen et al. (2008) demonstrated that the use of BFA had little effect on cross-presentation in immature DC and CpG-activated DC. This explained some described pathway, such as vacuolar and phagosome-to-cytosol-to-phagosome pathway did not use ER or Golgi for MHC-I presentation in certain APCs.

Up to 85% cross-presentation was blocked when TAP was inhibited by ICP47 expression in human DC (Fonteneau et al., 2003). TAP was needed in cross-presentation to transport antigens from cytosol into ER. Inhibition of TAP in DCs with US6 stopped the peptide loading on MHC-I molecules (Ackerman et al., 2005). There were some APCs still carried out cross-presentation when TAP was inhibited, and there were two possibilities for that which were some TAPs were not inhibited, or there were other routes that were TAP-independent. Cytoplasmic mutations in murine MHC class I cytoplasmic tail had no effect on fibroblasts transport of emerging MHC class I complexes, which migrated from ER through Golgi and to the cell surface (Lizee et al., 2003). Tapasin was not only also found important in bridging TAP and MHC-I molecules in mice, but was essential in stabilizing TAP (Garbi et al., 2003). Tapasin also found in TAP-deficient APCs but it was suggested that tapasin was not involved in fusion protein trafficking and processing (Tiwari et al., 2007).

Cross-Presentation and Vaccination
Knowing which cells present antigens, where does the cross-presentation occur in the body, and what antigens will be presented in certain routes help in better vaccine development. APCs’ molecular and cellular basis of cross-presentation need to be understood so that vaccine can be designed to delivered to cross-presentation APCs so that they can prime CTL.

Long cell surface lifetimes of MHC-I and delayed presentation of exogenous antigen can stimulate strong T cell response (Brophy et al., 2007). Vaccine can be designed to increase MHC-I lifetimes and delayed presentation of MHC-I. Factors that suppress cross-presentation can be studied and avoided in vaccination design. For example, increase adenosine (Ado) will suppress cross-presentation and consequently cause autoimmune response (Chen et al., 2008). The studies of how Ado levels affect CTL can be studies to optimize the effect of vaccines. Acidification affected endosomal functions in cross-presentation by human DC (Fonteneau et al.¸2003).

The cellular pH condition will also affect the cross-presentation by MHC-I molecules (Vermeulen et al., 2004). Inhibitions of vacuolar proton pump in mice also affect the endosomal activities (Tiwari et al., 2007). Vaccine can be designed to contain substances that can induce optimum pH condition in APCs so that activation of CTL can be improved.

As different antigens have different routes to process them to be presented in different APCs cross-presentation. Membrane-associated proteins were involved in TAP-independent pathway (Tiwari et al., 2007). Antigens used for vaccination could be enhanced to targeted specific APCs for better result. MHC-I molecules were found to be carriers of peptide epitopes, and vaccine can be manipulated to present suitable epitopes (Tiwari et al., 2007). Antigens can also be induced into other cells and present to APCs via gap junction (Neijssen et al., 2005). Vaccine can also be introduced to APCs via different methods that APCs take up antigens (Moron et al., 2004).

Proteasomes are also important in degrading antigens to be loaded on MHC-I. It was found that cathepsin D but now cathepsin B was responsible for cross-presentation enhancement in human DC (Fonteneau et al., 2003). This finding could also improve vaccination design which can be degraded by cathepsin D instead of cathepsin B. Understanding of HSP which can enhance antiviral and antibacterial immunity can also help to integrate HSPs into vaccine so that vaccine can be used to therapeutically generate stronger CTL responses (Tobian et al., 2004).

Conclusion
MHC-I molecules play a major role in cross-presentation. Cross-presentation is essential to activate CTLs in antiviral immunity. The intracellular routes of cross-presentation are still unclear. There are many things that can affect the result of experiment to define the routes, such as source of antigens, APCs used, and the source of organisms. There are many other cells other than DCs, can cross-present antigens to CTLs. More researches need to be done so that better vaccine can be developed to enhance CTL response.

References
Ackerman, A.L. and Cresswell, P. (2004), Cellular Mechanisms Governing Cross-Presentation of Exogenous Antigens, Nature Immunology, vol. 5, no. 7, pp. 678 – 684.

Ackerman, A.L., Giodini, A., and Cresswell, P. (2006), A Role for the Endoplasmic Reticulum Protein Retrotranslocation Machinery during Crosspresentation by Dendritic Cells, Immunity, vol. 25, pp. 607 – 617.

Ackerman, A.L., Kyritsis, C., Tampe, R., and Cresswell, P. (2005), Access of Soluble Antigens to the Endoplasmic Reticulum Can Explain Cross-Presentation by Dendritic Cells, Nature Immunology, vol. 6, no. 1, pp. 107 – 113.

Bevan, M.J. (1976), Cross-priming for a Secondary Cytotoxic Response to Minor H Antigens with H-2 Congenic Cells which do not Cross-React in the Cytotoxic Assay, Journal of Experimental Medicine, vol. 143, ppl. 1283 – 1288.

Brophy, S.E., Jones, L.L., Holler, P.D., and Kranz, D.M. (2007), Cellular Uptake Followed by Class I MHC Presentation of Some Exogenous Peptides Contributes to T Cell Stimulatory Capacity, Molecular Immunology, vol. 44, pp. 2184 – 2194.

Chen, L., Fredholm, B.B., Jondal, M. (2008), Adenosine, Through the A1 Receptor, Inhibits Vesicular MHC class I Cross-Presentation by Resting DC, Molecular Immunology, 2008, vol. 45, pp. 2247 – 2254.

Fonteneau, J.F., Kavanagh, D.G., Lirvall, M., Sanders, C., Cover, T.L., Bhardwaj, N. and Larsson, M. (2003), Characterization of the MHC Cass I Cross-Presentation Pathway for Cell-Associated Antigens by Human Dendritic Cells, Blood, vol. 102, pp. 4448 – 4455.

Freigang, S., Egger, D., Bienz, K., Hengartner, H., and Zinkernagel, R.M. (2003), Endogenous Neosynthesis vs. Cross-Presentation of Viral Antigens for Cytotoxic T Cell Priming, Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 23, pp. 13477 – 13482.

Garbi, N., Tiwari, N., Momburg, F., and Jammerling, G.J. (2003), A Major Role For Tapasin As A Stabilizer of the TAP Peptide Transporter and Consequences for MHC Class I Expression, European Journal of Immunology, vol. 33, pp. 264 – 273.

Guermonprez, P. and Amigorena, S. (2005), Pathways for Antigen Cross Presentation, Springer Seminar of Immunology, vol. 26, pp. 257 – 271.

Lizee, G., Basha, G., Tiong, J., Julien, J.P., Tian, M., Biron, K.E., and Jefferies, W.A. (2003), Control of Dendritic Cell Cross-Presentation by the Major Histocompatibility Complex Cass I Cytoplasmic Domain, Nature Immunology, vol. 4, no. 11, pp. 1065 – 1073.

Moron, G., Dadaglio, G. and Leclerc, C. (2004), New Tools for Antigen Delivery to the MHC Class I Pathway, Trends in Immunology, vol. 25, no. 2., pp. 92 – 97.

Neijssen, J., Herbets, C., Drifjhout, J.W., Reits, E., Janssen, L. and Neefjes, J. (2005), Cross-Presentation by Intercellular Peptide Transfer Through Gap Juntions, Nature, vol. 434, ppl. 83 – 88.

Norbury, C., Malide, D., Gibbs, J.S., Bennink, J.R. and Yewdell, J. (2002), Visualizing Priming of Virus-Specific CD8+ T Cells by Infected Dendritic Cells in invo, Nature Immunology, vol. 3, no. 3, pp. 265 – 271.

Shen, L. and Rock, K.L. (2006), Priming of T cells by Exogenous Antigen Cross-Presented on MHC Class I Molecules, Current Opinion in Immunology, vol. 18, pp. 85 – 91.

Shen, L., Sigal, L.J., Boes, M., and Rock, K.L. (2004), Important Tole of Cathepsin S in Generating Peptides for TAP-Independent MHC Class I Crosspresentation In Vivo, Immunity, vol. 21, pp. 155 – 165.

Tiwari, N., Garbi, N., Reinheckel, T., Moldenhauer, G., Hammerling, G.J., and Momburg, F. (2007), A Transporter Associated with Antigen-Processing Independent Vacuolar Pathway for the MHC Class I-Mediated Presentation of Endogenous Transmembrane Proteins, The Journal of Immunology, vol. 178, pp. 7932 – 7942.

Tobian, A.A.R., Canaday, D.H., Boom, H., and Harding, C. (2004), Bacterial Heat Shock Proteins Promote CD91-Dependent Class I MHC Cross-Presentation of Chaperoned Peptide to CD8+ T Cells by Cytosolic Mechanisms in Dendritic Cells versus Vacuolar Mechanisms in Macrophages, The Journal of Immunology, vol. 172, pp. 5277 – 5286.

Van Kaer, L. (2002), Major Histocompatiblity Complex Class I-restricted antigen processing and presentation, Tissue Antigens, vol. 60, pp. 1 – 9.

Vermeulen, M., Giordano, M., Trevani, A.S., Sedlik, C., Gamberale, R., Fernandez-Calotti, P., Salamone, G., Raiden, S., Sanjurjo, J., and Geffner, J.R. (2004), Acidosis Improves Uptake of Antigens and MHC Class I-Restricted Presentation by Dendritic Cells, The Journal of Immunology, vol. 172, pp. 3196 – 3204.

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I discovered Lab Bratz comic today.  It is pretty funny (I spent a day to finish all their comic).

This reminds me of the chemistry day.  I always lost count when someone interrupt me.

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Evolution is a fairy tale?

Chuck Missler misunderstood the whole theory of evolution. He thought peanut butter could grow mushroom. I won’t smile at that, but I will definitely laugh at THAT!

Facts:

1. Food industries spend billion dollars every year to make their food sterilized so that microorganisms won’t grow on it.
2. Food industries don’t depend on evolution doesn’t happen.
3. Peanut butter doesn’t made by crashing both peanuts and butter together.
4. Peanut butter is not as easy as you thought.
5. People won’t buy/eat peanut butter with other organisms.
6. Microorganisms grow on food when it is exposed to them, and when the condition is right (temperature, nutritions, acidicity, etc.), they will grow.
7. Organisms grow on sterilized peanut butter is a fairy tale.

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Many science students cannot accept science blogging (some not even give it a try for personal blogging), but there are a lot of benefits for a science student to write a blog. I had invited a lot of people to author in this blog, but I faced lots of rejections. The common excuses these people come up with are “bad language”, “not enough time”, “not a pro in science”, etc. Honestly, are those reasons matter? Here I list out the reasons why you should start science blogging.

1. You can improve your writing skills.

Language is learnt through practising. The more you write, the better your writing skill will be. Being poor in language is not an excuse not to start science blogging. Frankly, if you can’t even write a blog entry, how could you write science papers and reports? English is not the first language of most of the bloggers here, and we constantly making mistakes in our writings but we also improve our writings consistently.

2. Expanding your social circle.

Blogging is a tool you can use to connect yourself to another world. Maybe many scientists do not own a blog, but there are many who read blogs. Blog helps you in social networking. I met many people through blogging, and they are really helpful in term of helping me up in my assignments, answering my questions, introducing me jobs, etc. Besides, people I never know them before also contacted me via this blog. They corrected my mistakes, updating me with latest news and products, and also discussing things with me.

3. You read science news.

The cruel fact for most of the blogs is that if you don’t update your blog, you will lose your readers eventually. In order to update blogs, you need to find materials to write. One of the easiest things to write is updating your readers with latest science news. Having a blog allows you to read what is the latest updates in your field (as well as others), and you will not only be the nerds who only read the outdated textbooks.

4. You learn while you write.

Teaching is the best way of learning. When you start to teach something, that means that you understand it. You will also remember what you wrote down, and you may go to check if what you have written is correct. All these acts help you in learning and remembering things. As mentioned in reason #1, you also learn the writing skills.

5. Crap the stress out.

It’s good when you have someone to talk to so that you can destress yourself. What if you don’t have anyone to talk to or you are doing hell lots of assignments (while everyone else has loads of works too)? Blog will become one of the best tools to voice out yourself. You can also b*tch your lab partner or supervisor with blog. Don’t keep things in your heart. It’s unhealthy.

6. Time management.

Time is the reason why most science students say no to blogging. This is bullcrap! Blogging shows that you have good time management skill. Don’t make reports, assignments, lecture, studies, etc. become an excuse that you don’t have extra time. I believe many of you spend time on youtube more than assignments. Saying that you don’t have enough time is just showing that you are a loser. You can’t even manage your time properly.

7. Seek for answers.

Blog is a good platform for communication. Anyone can read your blog. Sometimes when you have doubts in your studies, please don’t hesitate to ask in your blog. There are a lot of people who knows the answer are willing to help you. As mentioned in reason #2, you can know people through blogging. There is always someone I can ask for solutions in my MSN list.

8. Kill time in lab.

Long incubation hours are a pain. Chit-chatting with lab partners or doing some readings are always a good way of killing those time. However some students, who are working alone in the lab, might not have people to talk to or don’t have anything else to do. Go for a coffee alone is pathetic. You can use this time to produce something productive via blogging (but please don’t leak your confidential research materials out).

9. Read blogs don’t belong to you.

In life, especially in the science field, you are constantly learning new things. When you get in touch with blog, you will eventually read others’ blogs. Many blogs have different opinions and latest updates in their field. You will find that science itself is like politics. It’s not as peaceful as what you read on textbook. Science is constantly changing. Different scientists have different opinions for different phenomenon. They constantly challenge studies done by others. What is not changing in Science is the changing itself. Besides knowing what others thoughts and opinions, reading also improve your language.

10. Sharing.

You had a good meal? You watched a really amazing movie? You met a really cute guy? You can share it in your blog. Science blogging doesn’t mean everything needs to be scientific jargon. It has nothing to do with IQ. I always write in this blog how much I enjoy sleeping in the lecture (I don’t mean it). Sharing is caring.

11. You got paid.

Face it. Money is the most useful thing in this world. Blogging can bring you little pocket money. You can have a various choices of way to earn money via blogging, such as adsense, selling text links, affliate products, reviews, etc. Every penny counts, especially when you are a student. Don’t waste your youth being a student who have negative value. Always try to earn some money when you are a student as you have most of the free time during this period of life.



12. Reduced your potential competitors.

Competitors! Those are the people who might fight for a job position with you in the future! The only way to get rid of them is making them choose other paths rather than science. Tell them how ugly laboratory politics is, how poor a scientist can be, how lonesome scientist is, etc. You can achieve this goal by blogging the dark sides of science.  You can also write a long dull post that bored your readers.

13. You Learn how to switch on your computer

Don’t freak out if you found out someone around you don’t know how to switch on a computer (or maybe you are the one). Blogging can teach you many typing skills, such as Ctrl + C for copy, Ctrl + i for italics, Ctrl + b for bold, etc. They are simple, and yet many people don’t master them.

Nerdy Science Blog welcomes anyone with science background join us for volunteer authoring, however reason #11 doesn’t apply on this blog. Please contact us if you are interested.

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