The Handkerchief of Love and Deception in Othello Essays

Othello and Desdemona started their life together thinking it was to be forever. The handkerchief symbolizes the start of a new generation, a token of their union and ultimately determines their fate and the main characters lives being changed by the events. The films adaption, as in Shakespeare play, he makes the handkerchief significant to the plot. Othello’s mother gave him the handkerchief on her dying bed to give to the women he marries. â€Å"She, dying, gave it me, and bid me, when my fate would have me wive; to give her.† Desdemona and Othello confess their love for one another in hopes of a blissful life together. Unbeknown to them that the handkerchief would be their down fall. Desdemona â€Å"The†¦show more content†¦(3.3 .279-289). Iago’s deceitfulness about the handkerchief affects Othello’s psychological thinking concerning Desdemona. Emilia has retrieves the handkerchief, leaves the room and goes to her husband to present the handkerchief. â€Å"How now? What do you hear alone?† Iago asks Emilia why are you here. â€Å"Do not you childe; I have a thing for you† you noble person, I have something for you. Emilia asked Iago what he is willing to do for the handkerchief that happens to be in her possession. Iago wants to know what she is talking about, Emilia replied the one gift that Othello has giving to his precious Desdemona. (3.3.290-308). Iago searches for the truth from Emilia and confides to Iago that Desdemona left the handkerchief by accident, which at this time I took the handkerchief. [Emilia holds the handkerchief up in the air.] Iago retrieve the handkerchief from Emilia and sniffs it, rolls over on top of her, speaks a few words and throws the handkerchief up in the air and made passionate love to his wife. Desdemona asks Emilia â€Å"Where should I lose that handkerchief, Emilia?† â€Å"I know not, madam.† Emilia lies about the handkerchief when asked by Desdemona. (3.4. 117). Othello comes into the room, ask Desdemona for thy hand and say, your hands areShow MoreRelatedEssay on Deception in Shakespeares Othello670 Words   |  3 PagesDeception in Shakespeare’s â€Å"Othello†   Ã‚  Ã‚  Ã‚  Ã‚  One may readily perceive the theme of Shakespeare’s â€Å"Othello† as deception. Deception appears many times in Othello, but in almost every incident the degree of deception is different. Deception is to â€Å"deceive another, illusion, or fraud† (Webster’s New World Pocket Dictionary 69), which is seen as a wrongful act. However, deception may be used to protect someone from getting hurt therefore being used with good intentions.   Ã‚  Ã‚  Ã‚  Ã‚  The very first act of deceptionRead MoreOthello - Deception and Vision Essay1500 Words   |  6 PagesDeception and Vision in Shakespeare’s Othello Walter Scott once stated, â€Å"Oh, what a tangled web we weave... when first we practice to deceive† (Quotation). 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Shakespeares Use of Madness as a Theme in King Lear

Edgar first assumes the disguise of Poor Tom as Lear and the Earl of Gloucester enter the cave in which Edgar is hiding. Since Edgar was banished, similar to Kent, who is also present later in this act, he must conjure up a disguise. Why does Edgar chose the repulsive beggar that Poor Tom is? Well, remember that Poor Tom represents the popular belief of the insane during the Elizabethan era. Therefore, he is the perfect disguise. No one would ever suspect Poor Tom of being Edgar, because Edgar is a very pleasant man, while Tom is completely repulsive. Furthermore, the reason Edgar chose this disguise is contained within his soliloquy as he is becoming Poor Tom: Whiles I may scape, I will preserve myself; and am bethought To take the†¦show more content†¦He is entertaining what he presumes will be the prevailing notion concerning the appearance and personality of the typical beggar, which is what Edgar has essentially been reduced to. Poor Tom is an incredibly repulsive character, who will receive no sympathy from the audience. However, the fact that Edgar has been reduced to this state will make the audience think, and potentially realize that anyone could be reduced this lowly state. After all, Edgar was one of the most noble and favored people in the kingdom. So, by making Edgar take on this disguise, Shakespeare could potentially cause the audience gain some sympathy for real life beggars. In addition, it could also potentially refute some of their beliefs concerning madness, and realize that they too could become mad, which in return should cause them to gain some sympathy for actual people who are mad. The reason that Shakespeare chooses Poor Tom to be Edgars disguise is to prove a major point concerning the origin of madness. Lear, the hero of the play, demonstrates to the audience Shakespeares beliefs concerning the true origin of madness. 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Mechanisms of Fear Memory Extinction and Psychological Therapeutic

Question: Discuss about the Mechanisms of Fear Memory Extinction and Psychological Therapeutic Approaches. Answer: Introduction: Fear is an emotion that exists in both human and animals, and it is easier to understand by studying brain mechanisms. In psychiatric conditions, the condition plays a critical role, and because of this, it is critical to understand its neural basis. Fear occurs when one is subjected to conditions that result into intimidating environmental states. Current research puts great emphasis on Pavlovian fear condition. This analysis involves measuring conditioned responses that an auditory conditioned stimulus exhibits when the memory test is underway, which is almost the same as real life experiences where an unconditioned stimulus (US) causes some harm and then the conditioned stimulus (CS) takes place about the painful stimulus. This is always the case when a cat wounds a rat but it escapes. The rat forms a memory of some noise or rustling of grass that occurred when the cat was about to pounce on it. This paper examines recent studies on both molecular and cellular mechanism that often result into auditory fear conditioning. While molecular changes do take place in many areas of the amygdala, the paper will focus on lateral (LA) nucleus as there is adequate prove that molecular change in this place contributes significantly to the acquisition, consolidation, and memory expression. Given that unique molecular mechanisms underscore stages of memory formation, this analysis will is based on Pavlovs dog and rodent research and is organized according to the three stages, acquisition, consolidation, and then reconsolidation of memories. Additionally, it presents the limitation of extinction. Pavlovs Dog Pavlov started the processes of discovering the Pavlovian conditioning theory when he saw a dog salivate. He first thought that dogs do not need to learn to do some things such as salivating when they see food. In behavioral terms, this means food is unconditional stimulus while salivating in unconditional response. Pavlov proved this is presenting his dog with a bowl of food and measuring its salivary secretions. Later, he also learned that the dog would produce the same amount of salivary secretions when it saw the lab assistant; he concluded that he had discovered a conditioned response. Pavlov chose to ring a bell whenever he presented the food. He recorded the same response (Pavlov, 1902). Memory exists when people learn. When observing molecules that initiate memory function, it appears true that there can be no memory whenever there is not learning as there is nothing to store in the brain. An understanding of LA mechanism of fear memory formation can help to appreciate how memory acquisition occurs. Consequently, it will analyze the application of rodent studies in humans followed by extinction-based strategies (Pavlov, 1902). Acquisition Stage The Hebbian mechanism, which is based on the findings of Hebb, is a common mechanism at this juncture. A common view based on it emerged in neuroscience that explains how a synaptic input can be enhanced (Learning Rule, 2008). This LA mechanism provides that when activities take place in the presynaptic neuron, a simultaneously activity occurs in the postsynaptic neuron, it becomes possible to strengthen a synaptic input. This relationship with the strong inputs strengthens the weak one (Kwok, 2009). One thing that Hebbian Plasticity does not guarantee, according to new evidence, is that LA can explain fear conditioning entirely (Pape and Pare, 2010). While Hebb explicitly explains how plasticity can occur during the acquisition stage, it fails to comprehensively explain learning, particularly learning that type of learning that occurs in highly charged emotional environments. This has led to the emergence of neuromodulatory-dependent mechanisms (Schiller et al., 2013). Recent research suggests that monoamine transmitters are responsible for regulating glutamatergic transmission as well as Hebbian plasticity (Tully and Bolshakov, 2010). Another credible evidence points to the fact that neuromodulatory regulation of this mechanism can lead to the development of plasticity and fear learning. Neurons in the LC, as well as substantial nigra, are activated by the USS and CSs. Consequently, after the presentation of aversive stimuli, the amount of NE and DA increases in the amygdala (Guzman-Karlsson et al., 2014). The conclusion here is that NE and DA have the ability to modulate the acquisition of fear learning. Consolidation Stage This term consolidation refers to the process of stabilization of temporary STMs into persistent STMs. Covalent modification of synaptic proteins is responsible for mediating plasticity that is essential for both STM and immediate learning. However, research has shown that the consolidation of this plasticity occurs through activation of second messengers. Alberini et al. (2009) provide that these messengers initiate the process of gene transcription and also a translation of new proteins. This research finding makes it clear that both neuromodulatory and Hebbian mechanisms play the role of implementing the original intracellular activities. However, they can as well prompt the sending of the messengers. As already indicated above, molecules that make STM possible are the ones involved in memory consolidation (Sacktor, 2008). Recent studies show that kinase is involved in memory maintenance. Sacktors works show that an atypical isoform of PKC is responsible for this task. Inhibition of this isoform in the LA after a fear learning experience clears fear memories (Sacktor, 2008). According to Jensen et al. (2009), it is true that the isoform of PKC maintains, and it may be doing this by reducing GluA2 AMPAR subunit removal, which ultimately results to the sustainability of the synaptic strengthening that the fear learning originally induced. Reconsolidation After learning, fear memories are consolidated and store. However, they can be labile when reconsolidated. During the process of reconsolidation, the presentation of memory that is related with the environmental cue, for example, conditioned CS to activate memories and that also makes them labile. If a behavioral manipulation following memory reactivation occurs following memory activation such as post-training manipulations, the new labile memory is transformed (Shih Wu, 2017; Agren et al., 2017). In many past instances, the study of reconsolidation has been undertaken through systematic pharmacological manipulations. A finding by Sara reveals that the disruption of the consolidation of STM is done by protein synthesis stoppage in the LA (Elsey Kindt, 2017). Schafe and his counterparts also led the research that discovered that blockade of protein synthesis also affected reconsideration adversely subsequent to the recovery of well-consolidated fear memories (Schafe et al., 2001). These series of research have caught the attention of many people. Researchers need to consider using auditory fear conditioning to examine these processes as the understanding about fear memory consolidation is at an advanced stage. However, going by the available research, it is apparent that blockade of reconsolidation helps to bring down auditory conditioned and unconditioned stimulus that is evoked by neural responses. This means that when reconsolidation is blocked, auditory thalamic inputs to LA neurons are potentiated (Alberini et al., 2013; Agren et al., 2017). The modification of the memory using reconsolidation-related extinction has provided several positive outcomes. Recent research has demonstrated how prefrontal cortex and hippocampus interact and affect memory retrieval and consolidation. In a successive Go/No-Go training of rats, Gilbert and Kesner (2004) investigated the role of the hippocampus and (medial prefrontal cortex) mPFC in spatial paired-associate learning. They discovered that rats with ibotenic acid-based lesions in the hippocampus had signs of irrecoverable performance impairment in location-in-place and object-in-place arms. However, when these researchers inactivated mPFC using muscimol in normal animals with intact hippocampi, the same severe impairment seen in object-in-place arms was registered. This experiment confirmed that the hippocampus is needed for a biconditional paired-associate task when space is required. On the other hand, the mPFC is more selectively involved in the object-pace paired-associate task than in any other tasks (Schiller at al., 2013). Contribution of Rodent Studies A lot of evidence suggests that fear memory reconsolidation can be blocked; the testing has been done on animals only. However, two recent studies have given encouraging results for reconsolidation of emotional memories in some patients as well as in healthy volunteers (Keum Shin, 2016). The slow pace of human reconsolidation research has been brought about by the fact that many compounds that are used to block reconsolidation in animals are toxic to humans. Besides, pharmacological agents could adversely affect different measures of fear in man (Schiller at al., 2013). The encouraging results in results led Schiller and his team to try to translate combined reconsolidation and extinction techniques to humans (Schiller at al., 2013). They successfully replicated the finding that extinction training carried out ten minutes after reactivation (the reconsideration window) reduced fear, but it did not lead to spontaneous recovery or returned following a reinstated shock. The reduction in fear achieved from the reconsolidation- extinction techniques took only one year and relapsed. From a clinical standpoint, the results are encouraging. However, as at now, it is impossible to tell whether the techniques can change traumatic memories in patients suffering from various traumatic disorders such as anxiety disorders (Agren et al., 2017). Using Extinction-based Therapies The boundary that has existed between the basic and clinical research has begun to become smaller given the development in extinction and reconsolidation research. The increasing use of DCS to facilitate extinction was developed from rodent studies. Today, they are showing promise in studies for social anxiety disorder, phobia, OCD, and PTSD. Since it strengthens extinction, pharmacologically adjusts can reduce the relapse of fear memory. As the rodent studies suggest, many other compounds are can be used to strengthen or accelerate extinction. Some of them, according to researchers Graham and Richardson (2010) are fibroblast growth factor, yohimbine, and methylene blue. Other recent studies may provide the solution. One of them has suggested that extinction can be adduced by purely pharmacological means (Lissek et al., 2013). The rodent studies revealed that extinction in young rodents led to paradoxical approach behaviors to the CS. When researchers conditioned rats to fear simple tones by associating them with electronic shock, they began the extinction phase. They discovered that more BLA-NAC activity could lead to extinction learning. When they gave rats food in the presences of the previously feared tone, this resulted in decreased spontaneous recovery of fear. The amygdala modulates the fear response in many functional magnetic resonance imagings (fMRI). This discovery can be used to treat childhood traumas. Research shows these strategies have been effective in children. The rodent study show that the development switches that control the permanence of these memories can be changed successfully (Lissek et al., 2013). The amygdale is well-known for playing a central role in the acquisition and expression of fear. Recent research has, however, implicated it in the extinction of fear memories. According to research, the amygdala corporate is regulated by the venromedial prefrontal cortex (PFCvm). When the hippocampus learns about the context of acquisition, it modulates the expression and extinction of the memories in relation to that particular context (Fuster, 2015). Limitations of Extinction Clinical treatment based on extinction has proven that this approach has several weaknesses. First, it relies on negative prediction errors that only be depended on if the CS predicted the US consistently. In most cases, highly feared outcomes take place infrequently or do not take place at all. A man who fears the heights, for example, can maintain fear despite never falling (Agren et al., 2017). The next limitation is that there is always a little correlation between memory strength and behavioral measures. A fear condition in rodents, for instance, clearly shows that between-session recovery of the CT cannot be predicted by within-session decreases in the CR. Extinction procedures also render the CS ambiguous. This may lead to unfavorable a situation for people with a verse ambiguity and uncertainty. Research has found that people with high self-reported intolerance of uncertainty express higher spontaneous recovery after extinction (Agren et al., 2017). Extinction can also relapse and is highly dependent on the context in which it occurs. By combining extinction and reconsolidation, it is possible to have a greater understanding of this concept. Intracellular processes can evidently interfere with reconsolidation after memory retrieval. However, there is also evidence that behavioral manipulations after memory reactivation can also change the memory of fear. A good example is extinction training. Through repeated presentation of the stimulus without using the US, this training helps to bring temporal memory extinction. If the same individual is exposed to a new context or the US, the memory can be revived. Extinction, therefore, often do not generalize beyond the therapy room, which is the cause of high relapse rates for PTSD and anxiety (Agren et al., 2017). Conclusion The last few decades have witnessed a significant increase in the interest of medical experts in the neural mechanisms of Pavlovian extinction. With adequate extinction, rats, people, and other subjects respond to the conditioned stimulus in a manner that suggests they have never been conditioned. As this analysis has demonstrated, many recent research studies have indicated that extinguished fear responses relapse following an aversive event, with time, or when the conditioned stimulus is presented in a different context, which is behavioral evidence that extinguishing fear does not erase all the memories. All it does is generate an inhibitory memory that temporarily suppresses the expression of fear. This paper has revealed that many modern researchers characterize the neural mechanism of inhibition, focus on the amygdala, hippocampus as well as prefrontal cortex to try to solve the problem of memory fears. Since this theory allows for a relapse, it is clearly not effective. The re medy, for that reason, is for experts to continue working on finding advanced behavioral methods that can modify the original fear memory permanently. References Agren, T., Bjrkstrand, J., Fredrikson, M. (2017). Disruption of human fear reconsolidation using imaginal and in vivo extinction. Behavioural Brain Research, 319, 9-15. doi:10.1016/j.bbr.2016.11.014 Alberini, C. M., Johnson, S. A., Ye, X. (2013). Memory Reconsolidation. Memory Reconsolidation, 81-117. doi:10.1016/b978-0-12-386892-3.00005-6 Elsey, J. W., Kindt, M. (2017). Tackling maladaptive memories through reconsolidation: From neural to clinical science. Neurobiology of Learning and Memory. doi:10.1016/j.nlm.2017.03.007 Fuster, J. M. (2015). Anatomy of the Prefrontal Cortex. The Prefrontal Cortex, 9-62. doi:10.1016/b978-0-12-407815-4.00002-7 Gilbert, P. E., Kesner, R. P. (2004, January). Memory for objects and their locations: the role of the hippocampus in retention of object-place associations. Retrieved May 13, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/14670357 Graham, B. M., Richardson, R. (2010). Fibroblast Growth Factor-2 Enhances Extinction and Reduces Renewal of Conditioned Fear. Neuropsychopharmacology, 35(6), 1348-1355. doi:10.1038/npp.2010.3 Guzman-Karlsson, M. C., Meadows, J. P., Gavin, C. F., Hablitz, J. J., Sweatt, J. D. (2014). Transcriptional and epigenetic regulation of Hebbian and non-Hebbian plasticity. Neuropharmacology, 80, 3-17. doi:10.1016/j.neuropharm.2014.01.001 Jensen, T. E., Maarbjerg, S. J., Rose, A. J., Leitges, M., Richter, E. A. (2009). Knockout of the predominant conventional PKC isoform, PKC, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake. AJP: Endocrinology and Metabolism, 297(2). doi:10.1152/ajpendo.90610.2008 Keum, S., Shin, H. (2016). Rodent models for studying empathy. Neurobiology of Learning and Memory, 135, 22-26. doi:10.1016/j.nlm.2016.07.022 Kwok, S. M. (2009). In vivo visualization of CaMKII activity in ocular dominance plasticity. Lissek, S., Glaubitz, B., Uengoer, M., Tegenthoff, M. (2013). Hippocampal activation during extinction learning predicts occurrence of the renewal effect in extinction recall. NeuroImage, 81, 131-143. doi:10.1016/j.neuroimage.2013.05.025 Nagarkatti, N., Deshpande, L., Delorenzo, R. (2009). PLASTICITY | The Role of Calcium in Mediating Neuronal Plasticity in Epileptogenesis. Encyclopedia of Basic Epilepsy Research, 1181-1189. doi:10.1016/b978-012373961-2.00324-6 Pape, H., Pare, D. (2010, April). Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856122/ Pavlov, I. P. (1902). The work of the digestive glands. London: Griffin. Sacktor, T. C. (n.d.). PKMzeta, LTP maintenance, and the dynamic molecular biology of memory storage. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/18394466 Schafe, G. E., Nader, K., Blair, H. T., LeDoux, J. E. (2001, September). Memory consolidation of Pavlovian fear conditioning: a cellular and molecular perspective. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/11506888 Schiller, D., Kanen, J. W., Ledoux, J. E., Monfils, M., Phelps, E. A. (2013). Extinction during reconsolidation of threat memory diminishes prefrontal cortex involvement. Proceedings of the National Academy of Sciences, 110(50), 20040-20045. doi:10.1073/pnas.1320322110 Shih, M., Wu, C. (2017). Gap Junctions Underlying Labile Memory. Network Functions and Plasticity, 31-50. doi:10.1016/b978-0-12-803471-2.00003-5 Tsukada, M. (2008). Interaction Between the Spatio-Temporal Learning Rule (Non Hebbian) and Hebbian in Single Cells: A Cellular Mechanism of Reinforcement Learning. INTECH Open Access Publisher. Tully, K., Bolshakov, V. Y. (2010, May 13). Emotional enhancement of memory: how norepinephrine enables synaptic plasticity. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/20465834

Look at Your Fish! by Samuel H. Scudder

'Look at Your Fish!' by Samuel H. Scudder Samuel H. Scudder (1837-1911) was an American entomologist who studied under the noted zoologist Jean Louis Rodolphe Agassiz (1807-1873) at Harvards Lawrence Scientific School. In the following narrative  essay, originally published anonymously in 1874, Scudder recalls his first encounter with Professor Agassiz, who subjected his research students to a rigorous exercise in close observation, analysis, and description  of details. Consider how the investigative process recounted here might be viewed as an aspect of critical thinking- and how that process can be just as important to writers as it is to scientists.   Look at Your Fish!* by Samuel Hubbard Scudder 1 It was more than fifteen years ago that I entered the laboratory of Professor Agassiz, and told him I had enrolled my name in the scientific school as a student of natural history. He asked me a few questions about my object in coming, my antecedents generally, the mode in which I afterward proposed to use the knowledge I might acquire, and finally, whether I wished to study any special branch. To the latter, I replied that while I wished to be well grounded in all departments of zoology, I purposed to devote myself specially to insects. 2 When do you wish to begin? he asked. 3 Now, I replied. 4 This seemed to please him, and with an energetic Very well, he reached from a shelf a huge jar of specimens in yellow alcohol. 5 Take this fish, said he, and look at it; we call it a haemulon; by and by I will ask what you have seen. 6 With that, he left me, but in a moment returned with explicit instructions as to the care of the object entrusted to me. 7 No man is fit to be a naturalist, said he, who does not know how to take care of specimens. 8 I was to keep the fish before me in a tin tray, and occasionally moisten the surface with alcohol from the jar, always taking care to replace the stopper tightly. Those were not the days of ground glass stoppers, and elegantly shaped exhibition jars; all the old students will recall the huge, neckless glass bottles with their leaky, wax-besmeared corks, half eaten by insects and begrimed with cellar dust. Entomology was a cleaner science than ichthyology, but the example of the professor, who had unhesitatingly plunged to the bottom of the jar to produce the fish, was infectious; and though this alcohol had a very ancient and fish-like smell, I really dared not show any aversion within these sacred precincts, and treated the alcohol as though it were pure water. Still, I was conscious of a passing feeling of disappointment, for gazing at a fish did not commend itself to an ardent entomologist. My friends at home, too, were annoyed, when they discovered that no eau de cologne would drown the perfume which haunted me like a shadow. 9 In ten minutes I had seen all that could be seen in that fish, and started in search of the professor, who had however left the museum; and when I returned, after lingering over some of the odd animals stored in the upper apartment, my specimen was dry all over. I dashed the fluid over the fish as if to resuscitate the beast from a fainting fit, and looked with anxiety for a return of the normal, sloppy appearance. This little excitement over, nothing was to be done but return to a steadfast gaze at my mute companion. Half an hour passed- an hour- another hour; the fish began to look loathsome. I turned it over and around; looked it in the face- ghastly; from behind, beneath, above, sideways, at a three-quarters view- just as ghastly. I was in despair; at an early hour I concluded that lunch was necessary; so, with infinite relief, the fish was carefully replaced in the jar, and for an hour I was free. 10 On my return, I learned that Professor Agassiz had been at the museum, but had gone and would not return for several hours. My fellow-students were too busy to be disturbed by continued conversation. Slowly I drew forth that hideous fish, and with a feeling of desperation again looked at it. I might not use a magnifying glass; instruments of all kinds were interdicted. My two hands, my two eyes, and the fish: it seemed a most limited field. I pushed my finger down its throat to feel how sharp the teeth were. I began to count the scales in the different rows until I was convinced that that was nonsense. At last a happy thought struck me- I would draw the fish, and now with surprise, I began to discover new features in the creature. Just then the professor returned. 11 That is right, said he; a pencil is one of the best of eyes. I am glad to notice, too, that you keep your specimen wet, and your bottle corked. 12 With these encouraging words, he added, Well, what is it like? 13 He listened attentively to my brief rehearsal of the structure of parts whose names were still unknown to me; the fringed gill-arches and movable operculum; the pores of the head, fleshy lips and lidless eyes; the lateral line, the spinous fins, and forked tail; the compressed and arched body. When I had finished, he waited as if expecting more, and then, with an air of disappointment: You have not looked very carefully; why, he continued, more earnestly, you havent even seen one of the most conspicuous features of the animal, which is as plainly before your eyes as the fish itself; look again, look again! and he left me to my misery. 14 I was piqued; I was mortified. Still more of that wretched fish! But now I set myself to my task with a will and discovered one new thing after another until I saw how just the professors criticism had been. The afternoon passed quickly, and when, towards its close, the professor inquired: 15 Do you see it yet? 16 No, I replied, I am certain I do not, but I see how little I saw before. 17 That is the next best, said he earnestly, but I wont hear you now; put away your fish and go home; perhaps you will be ready with a better answer in the morning. I will examine you before you look at the fish. 18 This was disconcerting; not only must I think of my fish all night, studying without the object before me, what this unknown but most visible feature might be; but also, without reviewing my new discoveries, I must give an exact account of them the next day. I had a bad memory; so I walked home by the Charles River in a distracted state, with my two perplexities. 19 The cordial greeting from the professor the next morning was reassuring; here was a man who seemed to be quite as anxious as I that I should see for myself what he saw. 20 Do you perhaps mean, I asked, that the fish has symmetrical sides with paired organs? 21 His thoroughly pleased Of course! of course! repaid the wakeful hours of the previous night. After he had discoursed most happily and enthusiastically- as he always did- upon the importance of this point, I ventured to ask what I should do next. 22 Oh, look at your fish! he said, and left me again to my own devices. In a little more than an hour he returned and heard my new catalog. 23 That is good, that is good! he repeated; but that is not all; go on; and so for three long days he placed that fish before my eyes; forbidding me to look at anything else, or to use any artificial aid. Look, look, look, was his repeated injunction. 24 This was the best entomological lesson I ever had- a lesson, whose influence has extended to the details of every subsequent study; a legacy the professor has left to me, as he has left it to many others, of inestimable value, which we could not buy, with which we cannot part. 25 A year afterward, some of us were amusing ourselves with chalking outlandish beasts upon the museum blackboard. We drew prancing star-fishes; frogs in mortal combat; hydra-headed worms; stately crawfishes, standing on their tails, bearing aloft umbrellas; and grotesque fishes with gaping mouths and staring eyes. The professor came in shortly after and was as amused as any at our experiments. He looked at the fishes. 26 Haemulons, every one of them, he said; Mr. - drew them. 27 True; and to this day, if I attempt a fish, I can draw nothing but haemulons. 28 The fourth day, a second fish of the same group was placed beside the first, and I was bidden to point out the resemblances and differences between the two; another and another followed, until the entire family lay before me, and a whole legion of jars covered the table and surrounding shelves; the odor had become a pleasant perfume; and even now, the sight of an old, six-inch, worm-eaten cork brings fragrant memories! 29 The whole group of haemulons was thus brought in review; and, whether engaged upon the dissection of the internal organs, the preparation and examination of the bony framework, or the description of the various parts, Agassizs training in the method of observing facts and their orderly arrangement, was ever accompanied by the urgent exhortation not to be content with them. 30 Facts are stupid things, he would say, until brought into connection with some general law. 31 At the end of eight months, it was almost with reluctance that I left these friends and turned to insects; but what I had gained by this outside experience has been of greater value than years of later investigation in my favorite groups.*This version of the essay Look at Your Fish! originally appeared in both  Every Saturday: A Journal of Choice Reading  (April 4, 1874) and the Manhattan and de la  Salle Monthly  (July 1874)  under the title In the Laboratory With Agassiz by A Former Pupil.