The Black Book Of Carmarthen Is The Oldest Surviving Manuscript Written Entirely In The Welsh Language.

+heroes of nusantara: multatuli

YES, I, Multatuli, “who have suffered much,”—I take the pen. I do not make any excuses for the form of my book,—that form was thought proper to obtain my object…. I will be read! Yes, I will be read. I will be read by statesmen who are obliged to pay attention to the signs of the times; by men of letters, who must also look into the book of which so many bad things are said; by merchants, who have an interest in the coffee auctions; by lady’s-maids, who read me for a few farthings; by governors-general in retirement; by ministers who have something to do; by the lackeys of these Excellencies; by mutes, who, more majorum, will say that I attack God Almighty, when I attack only the god which they made according to their own image; by the members of the representative chambers, who must know what happens in the extensive possessions over the sea which belong to Holland….  

Ay, I shall be read!

Eduard Douwes Dekker was born in Amsterdam, March 2nd 1820. His father was a ship’s captain and intended for his son to have a career in trade. This humdrum prospect disgusted Douwes Dekker and in 1838 he obtained a post as a civil servant on the island of Java. During the period between 1848 and 1851 Douwes Dekker eventually rose to serve as assistant resident in various regencies in the Indonesian archipelago including Natal, North Sumatra, Manado in Sulawesi and Ambon in the Moluccas. In 1857 he was transferred to Lebak, in the Bantam residency of Java (now Banten province). By this time, however, all the secrets of Dutch administration were known to him, and he had begun to openly protest about the abuses of the colonial system. Consequently, he was threatened with dismissal from his office for his openness of speech. Douwes Dekker resigned his appointment and returned to the Netherlands.

He was determined to expose in detail the scandals he had witnessed, and he began to do so in newspaper articles and pamphlets. Little notice, however, was taken of his protestations until, in 1860, he published his novel Max Havelaar under the pseudonym of Multatuli. Douwes Dekker’s new pseudonym, which is derived from Latin, means, “I have suffered much”, or, more literally “I have borne much” referring to himself, as well as, it is thought, to the victims of the injustices he saw. An attempt was made to suppress the inflammatory book, but in vain; it was read all over Europe. Apologists for colonialism accused Douwes Dekker’s horrific depictions of being exaggerated.

[ his statue in amsterdam ]

Although it was translated into English in 1868, the text wasn’t available in the author’s home country until over a century later in 1972. Collectively, Multatuli’s Max Havelaar has been translated into 34 different languages worldwide since its initial publication. Credited as the stirring initiation of the nationalist movement responsible for the termination of Dutch colonization of Indonesia following World War II, Max Havelaar’s legacy is not confined to literary accomplishment, but can be considered a work of great political success and inspired social liberation. Max Havelaar’s influence on the national movement ultimately culminated in the passionate command to end decolonization worldwide. The story of Max Havelaar illuminates the inhumane and political injustices brutally imposed upon the native peoples of the region.

Sigmund Freud listed Multatuli as one of his favorite writers. Multatuli’s brother, Jan Douwes Dekker, was the grandfather of Ernest Douwes Dekker (also known as Danudirja Setiabudi, a National Hero of Indonesia). There is a museum for him in Amsterdam. Multatuli is also known as the person who coined the term emerald of equator, a poetic nickname of Indonesia.

This book is an introduction….  I shall increase in strength and sharpness of weapons, according as it may be necessary.    Heaven grant that it may not be necessary!…    No, it will not be necessary! For it is to thee I dedicate my book: WILLIAM THE THIRD, King, Grand Duke, Prince,… more than Prince, Grand Duke, and King,… EMPEROR of the magnificent empire of INSULIND, which winds about the equator like a garland of emeralds!…    I ask THEE if it be thine IMPERIAL will that the Havelaars should be bespattered with the mud of Slymerings and Drystubbles; and that thy more than thirty millions of SUBJECTS far away should be ill treated and should suffer extortion in THY name!

source: wikipedia; culture trip

quotes from bartleby, excerpt of max havelaar

further reading: paper on multatuli

First genetic proof that women were Viking warriors

New DNA evidence uncovered by researchers at Uppsala University and Stockholm University shows that there were in fact female Viking warriors. The remains of an iconic Swedish Viking Age grave now reveal that war was not an activity exclusive to males – women could be found in the higher ranks at the battlefield.

The study was conducted on one of the most well-known graves from the Viking Age, a mid-10th century grave in Swedish Viking town Birka. The burial was excavated in the 1880s, revealing remains of a warrior surrounded by weapons, including a sword, armour-piercing arrows, and two horses. There was also a full set of gaming pieces and a gaming board.

The morphology of some skeletal traits have long suggested that she was a woman, but since this grave has been the type specimen for a Viking warrior for over a century, it has always been assumed to have belonged to a male Viking. Now, geneticists, archaeogeneticists and archaeologists have worked together and solved the mystery. DNA retrieved from the skeleton demonstrates that the individual carried two X chromosomes and no Y chromosome. Read more.

Meet the orchid mantis.

Orchid mantises—particularly juveniles—seem aptly named. They’re predominantly white with pink or yellow accents, similar to some orchids and other flowers, and their four hind legs are lobed, like petals. But if you search for an exact floral counterpart, as behavioral ecologist James O’Hanlon did, you probably won’t find one. “I spent forever looking for a flower that they look just like,” he says, to no avail.

As it turns out, rather than mimicking one floral species, the insect instead may embody a “generic or an average type of flower” in order to attract bees and other pollinating insects as prey.

What’s more, as far as O’Hanlon can tell, it’s the only animal on record that “takes on the guise of a whole flower blossom” as a predatory strategy. 

Learn more here.

Neuro chip records brain cell activity at higher resolution

Brain functions are controlled by millions of brain cells. However, in order to understand how the brain controls functions, such as simple reflexes or learning and memory, we must be able to record the activity of large networks and groups of neurons. Conventional methods have allowed scientists to record the activity of neurons for minutes, but a new technology, developed by University of Calgary researchers, known as a bionic hybrid neuro chip, is able to record activity in animal brain cells for weeks at a much higher resolution. The technological advancement was published in the journal Scientific Reports.

“These chips are 15 times more sensitive than conventional neuro chips,” says Naweed Syed, PhD, scientific director of the University of Calgary, Cumming School of Medicine’s Alberta Children’s Hospital Research Institute, member of the Hotchkiss Brain Institute and senior author on the study. “This allows brain cell signals to be amplified more easily and to see real time recordings of brain cell activity at a resolution that has never been achieved before.”

The development of this technology will allow researchers to investigate and understand in greater depth, in animal models, the origins of neurological diseases and conditions such as epilepsy, as well as other cognitive functions such as learning and memory.

“Recording this activity over a long period of time allows you to see changes that occur over time, in the activity itself,” says Pierre Wijdenes, a PhD student in the Biomedical Engineering Graduate Program and the study’s first author. “This helps to understand why certain neurons form connections with each other and why others won’t.”

The cross-faculty team created the chip to mimic the natural biological contact between brain cells, essentially tricking the brain cells into believing that they are connecting with other brain cells. As a result, the cells immediately connect with the chip, thereby allowing researchers to view and record the two-way communication that would go on between two normal functioning brain cells.

“We simulated what Mother Nature does in nature and provided brain cells with an environment where they feel as if they are at home,” says Syed. “This has allowed us to increase the sensitivity of our readings and help neurons build a long-term relationship with our electronic chip.”

While the chip is currently used to analyze animal brain cells, this increased resolution and the ability to make long-term recordings is bringing the technology one step closer to being effective in the recording of human brain cell activity.

“Human brain cell signals are smaller and therefore require more sensitive electronic tools to be designed to pick up the signals,” says Colin Dalton, adjunct professor in the Department of Electrical and Computer Engineering at the Schulich School of Engineering and a co-author on this study. Dalton is also the facility manager of the University of Calgary’s Advanced Micro/nanosystems Integration Facility (AMIF), where the chips were designed and fabricated.

Researchers hope the technology will one day be used as a tool to bring personalized therapeutic options to patients facing neurological disease.

The late effects of stress: New insights into how the brain responds to trauma

Mrs. M would never forget that day. She was walking along a busy road next to the vegetable market when two goons zipped past on a bike. One man’s hand shot out and grabbed the chain around her neck. The next instant, she had stumbled to her knees, and was dragged along in the wake of the bike. Thankfully, the chain snapped, and she got away with a mildly bruised neck. Though dazed by the incident, Mrs. M was fine until a week after the incident.

Then, the nightmares began.

She would struggle and yell and fight in her sleep every night with phantom chain snatchers. Every bout left her charged with anger and often left her depressed. The episodes continued for several months until they finally stopped. How could a single stressful event have such extended consequences?

A new study by Indian scientists has gained insights into how a single instance of severe stress can lead to delayed and long-term psychological trauma. The work pinpoints key molecular and physiological processes that could be driving changes in brain architecture.

The team, led by Sumantra Chattarji from the National Centre for Biological Sciences (NCBS) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem), Bangalore, have shown that a single stressful incident can lead to increased electrical activity in a brain region known as the amygdala. This activity sets in late, occurring ten days after a single stressful episode, and is dependent on a molecule known as the N-Methyl-D-Aspartate Receptor (NMDA-R), an ion channel protein on nerve cells known to be crucial for memory functions.

The amygdala is a small, almond-shaped groups of nerve cells that is located deep within the temporal lobe of the brain. This region of the brain is known to play key roles in emotional reactions, memory and making decisions. Changes in the amygdala are linked to the development of Post-Traumatic Stress Disorder (PTSD), a mental condition that develops in a delayed fashion after a harrowing experience.

Previously, Chattarji’s group had shown that a single instance of acute stress had no immediate effects on the amygdala of rats. But ten days later, these animals began to show increased anxiety, and delayed changes in the architecture of their brains, especially the amygdala.

“We showed that our study system is applicable to PTSD. This delayed effect after a single episode of stress was reminiscent of what happens in PTSD patients,” says Chattarji. “We know that the amygdala is hyperactive in PTSD patients. But no one knows as of now, what is going on in there,” he adds.

Investigations revealed major changes in the microscopic structure of the nerve cells in the amygdala. Stress seems to have caused the formation of new nerve connections called synapses in this region of the brain. However, until now, the physiological effects of these new connections were unknown.

In their recent study, Chattarji’s team has established that the new nerve connections in the amygdala lead to heightened electrical activity in this region of the brain.

“Most studies on stress are done on a chronic stress paradigm with repeated stress, or with a single stress episode where changes are looked at immediately afterwards – like a day after the stress,” says Farhana Yasmin, one of the Chattarji’s students. “So, our work is unique in that we show a reaction to a single instance of stress, but at a delayed time point,” she adds.

Furthermore, a well-known protein involved in memory and learning, called NMDA-R has been recognised as one of the agents that bring about these changes. Blocking the NMDA-R during the stressful period not only stopped the formation of new synapses, it also blocked the increase in electrical activity at these synapses.

“So we have for the first time, a molecular mechanism that shows what is required for the culmination of events ten days after a single stress,” says Chattarji. “In this study, we have blocked the NMDA Receptor during stress. But we would like to know if blocking the molecule after stress can also block the delayed effects of the stress. And if so, how long after the stress can we block the receptor to define a window for therapy,” he adds.

Chattarji’s group first began their investigations into how stress affects the amygdala and other regions of the brain around ten years ago. The work has required the team to employ an array of highly specialised and diverse procedures that range from observing behaviour to recording electrical signals from single brain cells and using an assortment of microscopy techniques. “To do this, we have needed to use a variety of techniques, for which we required collaborations with people who have expertise in such techniques,” says Chattarji. “And the glue for such collaborations especially in terms of training is vital. We are very grateful to the Wadhwani Foundation that supports our collaborative efforts and to the DBT and DAE for funding this work,” he adds.

Molecule of the Day: VX

VX (C11H26NO2PS) is a colourless, odourless, oily liquid under room temperatures. It is a member of the V-series of nerve agents, and is an extremely potent poison - only 0.01 grams of it is needed to kill a person by skin contact. VX was recently implicated in the assassination of Kim Jong-nam, the half-brother of the North Korean leader Kim Jong-un, in Malaysia.

VX is a potent inhibitor of acetylcholinesterase, which breaks down the neurotransmitter acetylcholine into acetic acid and choline. The normal function of the enzyme is to regulate the concentration of acetylcholine within the synaptic cleft, so as to control the frequency of binding of acetylcholine to cholinergic receptors on the postsynaptic cell membrane and hence the transmission of impulses across the synapse.

Consequently, the inhibition of acetylcholinesterase results in a rapid increase in the synaptic concentration of acetylcholine, as the presynaptic knob continues to synthesise it and secrete it into the synaptic cleft. As a result, the cholinergic receptors on the postsynaptic cell membrane are continually stimulated, and a rapid series of action potentials are triggered. This results in muscle spasms and eventual paralysis, leading to death by asphyxiation due to paralysis of the diaphragm.

VX exposure is usually treated using an injection of atropine and pralidoxime. Atropine inhibits certain cholinergic receptors, reducing the binding of acetylcholine to receptors and thus the triggering of action potentials. On the other hand, one end of pralidoxime binds to acetylcholinesterase and the other binds to the phosphate group of VX, which causes the VX molecule to detach from the enzyme together with the pralidoxime molecule (see below). This restores the ability of acetylcholinesterase to hydrolyse acetylcholine, hence reducing its synaptic levels.

VX is synthesised from phosphorus trichloride over multiple steps; first, it is methylated, reacted with ethanol, then transesterified with N,N-diisopropylaminoethanol to produce QL. This is then oxidised with sulfur, and isomerised via heating to produce VX.

Knowing the 20 Amino Acids is definitely a MUST for the 2015 MCAT 

Amino acids that are usually negative (i.e. de-protonated) at physiological pH:

- Glutamate (E) Glu, and Aspartate (D) Asp

Amino acids that are usually positive (i.e. protonated) at physiological pH:

- Lysine (K) Lye, Arginine ® Arg 

Histidine is sometimes charged at physiological pH. 

physiological pH = 7, Neutral 

My boyfriend, @inlove-with-a-spine, is very uninformed about Southeast Asian fruits (he only knows durian) which inspired me to find these online.

I’m pretty sure the names are different in other Southeast Asian countries, though.

From left to right (in Indonesian):

Duku

Jambu monyet

Jeruk

Lengkeng

Kedondong

Manggis

Rambutan

Nangka

Salak

Sawo

Hey resident neuroscientist @sixpenceee, wanna explain why the strawberries look red?