Creatinine Lab

Title: Creatinine Assay Aim: To decide the creatinine freedom of a chose undiluted pee tests by graphical extrapolation from a creatinine bend. Materials and Apparatus: University of the West Indies: Department of Basic Medical Sciences Laboratory Manual: BC35A, Creatinine Assay, pages 6-8, 2012 Changes to the Method: The examination used one undiluted pee tests for focus assurance rather than five aliquots of twenty four hour pee samples.The pee test and standard creatinine arrangements were broke down spectrophotometrically roughly five minutes after they were made up as opposed to utilizing the distributed time stretch (minutes) as recommended by the research facility manual. Results: Please observe connections. Conversation Creatinine is a compound waste particle that is produced from muscle digestion. It is an anhydride of creatine, the finished result of phosphocreatine digestion; estimations of its pace of urinary discharge are utilized as symptomatic pointers of kidney capaci ty and bulk. The test used serum creatinine.Creatinine is sifted through of the blood by the kidneys (glomerular filtration). There is minimal cylindrical reabsorption of creatinine. In the event that the separating of the kidney is inadequate, creatinine blood levels rise. In this way, creatinine levels in blood and pee might be utilized to ascertain the creatinine leeway which mirrors the glomerular filtration rate (GFR). The GFR is clinically significant in light of the fact that it is an estimation of renal capacity . An increasingly complete estimation of renal capacity can be made when deciphering the blood (plasma) centralization of creatinine alongside that of urea.BUN-to-creatinine proportion (the proportion of blood urea nitrogen to creatinine) can show different issues other than those natural for the kidney; for instance, a urea level raised messed up with regards to the creatinine may demonstrate a pre-renal issue, for example, volume exhaustion. The normal human refere nce ranges for serum creatinine are 0. 5 to 1. 0 mg/dl (around 45-90 ? mol/l) for ladies and 0. 7 to 1. 2 mg/dl (60-110 ? mol/L) for men. While a pattern serum creatinine of 2. 0 mg/dl (150 ? mol/l) may show ordinary kidney work in a male body builder.The exploratory creatinine levels acquired for the undiluted example of creatinine is ____________, the qualities got are altogether higher than the typical creatinine values for a sound male or female. Elements that may add to the raised degrees of serum creatinine may incorporate; a turmoil of the kidneys and disabled renal capacity. These disarranges incorporate glomerulonephritis portrayed by aggravation of the veins in the kidneys, bacterial contamination of the kidneys or pyelonephritis and intense rounded corruption, or cell demise in the kidneys' little cylinders brought about by harmful substances.Obstruction of the urinary tract, for example, with prostate infection or kidney stones, can likewise cause disabled kidney capacit y and lead to raised creatinine levels. Expanded bulk shows expanded creatine phosphate, which means expanded creatinine levels in the blood. Acromegaly and gigantism are disarranges brought about by irregularity of the pituitary organ and can be related with expanded bulk likewise the ingestion of steroidal substances that invigorates an expansion in muscle mass.When ailments influence ordinary blood stream to the kidneys, renal capacity becomes impeded consequently expanding creatinine levels in the blood. Stun, or an abrupt basic drop in blood stream to the body, bargains renal status in light of the fact that the kidneys are not being fed. Drying out causes diminished renal blood stream, also. In individuals with congestive cardiovascular breakdown, the heart isn't sufficiently siphoning blood towards the kidneys and different organs. Atherosclerosis, or narrowing of the veins, and diabetic nephropathy are different conditions that lessen blood stream to the kidneys.Precautions/ Sources of Error: 1. The examination use spectrophotometric machines that are vulnerable to light interfence from the outside condition and impedance from dishes that isn't appropriately cleaned, this may cause wrong readings. 2. Defilement of serum standard arrangements of creatinine may give incorrect readings when utilizing the spectrophotometric machines, henceforth pollution ought to be forestalled by utilizing clean dish sets and wearing all the ensured dress that is appropriate. Questions a) Factors that may add to differing creatinine levels include: (1)The most normal variation from the norm in a creatinine blood level is an adjustment in kidney work. The kidneys are made out of around a million channels for every kidney, called nephrons. Every one of these nephrons contains rounded structures that achieve the separating of waste materials and the re-retention of fundamental materials in the blood that went through the nephrons. Most creatinine is typically sifted through a long two structures called the glomerulus and proximal tangled tubule, keeping up the low degrees of creatinine in the blood.A ascend in creatinine blood levels demonstrates that this filtration isn't occurring, recommending there is an issue with kidney work. (2) Creatinine levels can be influenced by transient or non-malady factors that are not kidney glitch. Weight lifters, as a result of the abundance of solid tissue that makes creatinine, will ordinarily have elevated levels of creatinine. Serious lack of hydration will cause higher than typical creatinine. Eating a lot of meat only hours before blood is drawn can hoist creatinine levels.Some medications will cause higher than ordinary creatinine blood levels. These causes are precluded before a subsequent test to decide the reason for raised creatinine. Low creatinine levels may demonstrate solid dystrophy or myasthenia gravis. (3) Preeclampsia is a condition during pregnancy, the reason for which is inadequately comprehended. Raised creatinine may demonstrate preeclampsia in pregnant ladies, particularly ladies on their first pregnancy. Untreated preeclampsia can prompt eclampsia, a hazardous seizure disorder.Elevated creatinine related to growing of the hands and face is an early indication of preeclampsia. Later signs may incorporate tenacious cerebral pain, torment in the upper-right quadrant of the midsection, deficient pee, unsettling and sickness. 2b) The measure of creatinine the body delivers every day relies upon the individual's bulk: a youthful, solid man creates more creatinine than a normal non athletic male. Since bulk ordinarily changes practically nothing, creatinine is generally delivered at about a similar rate each day in each person.However, if ceaseless exercise is proceeded as on account of a competitor the muscle utilizes the creatine phosphate digestion all the more frequently and henceforth more creatine and creatinine is used which will in the end increment the bulk of the pers on. Competitors may likewise ingest creatine which will invigorate the creation of creatinine in the body and will add to an expansion in bulk. 2c) The blood urea test is a proportion of the measure of nitrogen in the blood as urea, and an estimation of renal function.Urea is a result from digestion of proteins by the liver and is expelled from the blood by the kidneys. The liver produces urea in the urea cycle as a waste result of the assimilation of protein. Ordinary human grown-up blood ought to contain between 7 to 21 mg of urea nitrogen per 100 ml (7â€21 mg/dL) of blood. BUN means that renal wellbeing. Ordinary extents 2. 5-6. 5mmol/L. On the off chance that Glomerular Filtration Rate (GFR) and blood volume then BUN will increment. End The trial results show that there was a raised serum creatinine level that was over the typical levels.Elevated serum fixation may demonstrate debilitated liver capacity. The serum creatinine level was seen as ______________. References 1. Del anghe J; De Slypere JP, De Buyzere M, Robbrecht J, Wieme R, Vermeulen An (Aug 1989). â€Å"Normal reference esteems for creatine, creatinine, and carnitine are lower in vegetarians†. Retreived October 3, 2012. 2. â€Å"The creatine-creatinine balance. The clear separation constants of creatine and creatinine. Recovered October 3, 2012. 3. â€Å"International Society of Sports Nutrition position stand: creatine supplementation and exercise†. October 3, 2012.

Wellness Tourism Essay Example

Wellbeing Tourism Essay The Holistic Approach Of Ayurveda Based Wellness Tourism In Kerala RAMESH U *Assistant Professor, College of Engineering, Munnar, Kerala Tel: 04865 230606,232989 (Off), Mob: 094472 46162, Fax: 04865 232106 E Mail : [emailprotected] com ABSTRACT Wellness, as a rule, is utilized to mean a sound parity of the psyche, body and soul that outcomes in a general sentiment of prosperity. It is a multidimensional condition, portraying the presence of positive wellbeing in a person as exemplified by personal satisfaction. Wellbeing/Wellness the travel industry alludes to trips that are taken by visitors with the rule intention being to improve their wellbeing and additionally prosperity. The wide utilization of elective drugs makes India an especially fascinating goal, and can charge itself as a comprehensive wellbeing arrangement. Kerala has been notable for a long time for its act of Ayurveda-an arrangement of medication that accepts not just getting the sickness however going to the entire individual. Keralas equable atmosphere, regular bounty of woodlands (with an abundance of herbs and therapeutic plants) and the cool rainstorm season (June November) are most appropriate for corrective and helpful bundles. Previously or after their treatmentâ€or bothâ€medical voyagers can appreciate Kerala’s numerous famous vacationer goals. Regardless of whether they appreciate legacy the travel industry, or survey natural life, a sea shore excursion, or back water encounters, Kerala has a lot to offer. The idea of wellbeing occasion, presently also called Wellness occasion, depends on the standards of Ayurveda, reflection, yoga, physical activities and a decent eating routine. We will compose a custom exposition test on Wellness Tourism explicitly for you for just $16.38 $13.9/page Request now We will compose a custom paper test on Wellness Tourism explicitly for you FOR ONLY $16.38 $13.9/page Recruit Writer We will compose a custom paper test on Wellness Tourism explicitly for you FOR ONLY $16.38 $13.9/page Recruit Writer It resembles restoration and tidy up process on all levels physical, mental and enthusiastic. Ayurveda manages measures for invigorating living during the whole range of life and its different stages. Furthermore, managing standards for support of wellbeing, it has additionally built up a wide scope of remedial measures to battle ailment. The fundamental goal of this paper is to dissect the explanation concerning why Kerala is being picked as a favored goal for Wellness Tourism and to investigate the present chances and offices offered to the Wellness searchers. Catchphrases: Well being, Health occasion, Ayurveda, Rejuvenation. Presentation More than 50 years prior, the World Health Organization characterized wellbeing as more than opportunity from ailment, infection, and incapacitating conditions (WHO, 1947). The proposal by World Health Organization that wellbeing had a positive segment prompted the utilization of the term wellnessâ€now generally used to portray the condition speaking to that positive segment (Corbin, Pangrazi, Franks, 2000). Halbert Dunn built up the way of thinking of wellbeing the travel industry to delineate about an exceptional condition of wellbeing including a general feeling of prosperity which considers man to be comprising of body, soul, mind and being reliant on his condition (Dunn, H. L, 1965). It is an idea that is appealing to guests who love consolidating prosperity and way of life human services administrations with the powerful urge to travel abroad. The worldwide headway in clinical research and innovations, expanded facililities of transportation and request of quick quality human services have given the patients worldwide to travel abroad for medicines. The Indian social insurance industry has understood the capability of this specialty showcase and has started to tailor their administrations for global guests (Ilyas, 2008). Government and private area concentrates in India gauge that clinical the travel industry could bring between $1 billion and $2 billion US into the nation by 2012. The reports gauge that clinical the travel industry to India is developing by 30 percent a year. So as to qualify as a contemporary health the travel industry experience, we would fight that some intentional commitment must be made to mental, otherworldly or enthusiastic prosperity notwithstanding physical. This takes health the travel industry from the domain of being simply a latent type of the travel industry with an attention on idealism to one where visitors are intentionally determined by the craving to effectively look for improved wellbeing. Apparently, notwithstanding, there had been a phenomenal increase in the quest for health throughout the entire existence of Tourism in the ongoing years (Smith Kelly, 2006). The current pattern, in any case, is for western visitors to look for comfort in Eastern ways of thinking and treatments (e. g. , Chinese medication, Buddhist reflection, Indian Ayurveda, Thai back rub). With more individuals in the west understanding the adequacy of customary and regular meds in treating ceaseless ailments over present day prescriptions utilizing synthetic medications, the degrees gave by Kerala is getting a high ground in the Modern world. The Ayurvedic arrangement of medication has gotten mainstream among sightseers in the ongoing occasions. Ayurveda has its own extensive method of understanding the body, of what causes infections, how to forestall them, how to ease and fix them, techniques for getting ready restorative meds utilizing herbs and oils, revival and strategies for medical procedure. Kerala is the main spot where Ayurveda is drilled in its actual and genuine structure. Wellbeing related the travel industry administrations gave by Kerala are presently the most discussed point among the sightseers and medicinal services the travel industry providers’ around the world. The reason for this paper is to feature the all encompassing methodology offered to the health searchers visiting Kerala through the conventional treatments and the components that continue this one of a kind the travel industry item. Conversation Health is inherent and a characteristic wonder. It is a law of the nature to shield the individuals from sicknesses. The quick paced way of life and upsetting employment combined with absence of activity and over the top dietary patterns have made the cutting edge official human to an assortment of diseases. Despite the fact that the mechanical progression of present day medication is colossal, its ability for controlling and forestalling infections has gone down significantly. Individuals are taking much more of medications than they used to, and tranquilize costs are blowing up at a higher rate than some other segment of social insurance (Angel, 2004). There have been a few endeavors to order explicit proportions of Wellness, such factors as close to home vitality, capacity to appreciate relaxation, better mental self view and self-assurance, to name yet a few(Cooper, 1982). Clinical the travel industry can be comprehensively characterized as arrangement of savvy private clinical consideration in a joint effort with the travel industry for patients requiring careful and different types of particular treatment. The travel industry in its underlying stages was legitimately planned for expanding wellbeing and prosperity of individuals. In the current decade, the endeavor to accomplish better wellbeing while on a vacation through unwinding, exercise or visits to spas has been taken into another level, with the rise of an unmistakable specialty in the travel industry, â€Å"Wellness Tourism†, where the travel industry is intentionally connected to coordinate wellbeing intercessions and the results are relied upon to be considerable. The developing overall spotlight on wellbeing and prosperity has prompted a tremendous increment in the health offices in India. The country’s National Health Policy proclaims that treatment of outside patients is lawfully a fare nd regarded qualified for every financial motivator stretched out to send out income. The expanding allure and financial centrality of wellbeing and Wellness the travel industry is further clear in the development of both local and global guests since the start of this decade. India is the most touted human services goal for nations like South-East Asia, Middle East, Africa, Mauritius, Tanzania, Bangladesh and Yemen with 12 percent tolerant inflow from creating nations. An expected 150,000 clinical visitors visited India during 2007, speaking to a 20% hop over the earlier year and reports uncover that the income from Ayurveda Tourism alone added up to Rs 60 billion. Table 1 demonstrates the remote traveler appearances and the outside trade income from 1996 to 2006. India has a tremendous decent variety of occasion alternatives extending from the sea shores of Goa, the forceful Himalayas, a large number of long stretches of culture, assorted untamed life and obviously the Ayurveda based health offices offered by Kerala. The additional attractions to patients who wish to profit treatment in India is clinical visa, it will presently be simpler to head out to India as the visa could be stretched out with no issue. Aside from the serious valuing and specific Medicare facililities, the Ayurveda based customary medicines offered by Kerala has now risen as the USP for India to create as the most looked for after human services goal in the World. Ayurveda based Wellness offices Offered by Kerala †The entrancing area situated in the south of India appreciates geological highlights that are novel and rich. Kerala is one of only a handful hardly any honored grounds on the planet that is arranged by forty four streams. These streams are otherwise called the â€Å"backwaters of Kerala† and it extends up to just about 1900 kilometers. Kerala has a portion of the astonishing, most enchanting sea shores of the world. The brilliant sea shores consistently remain washed in the brilliant beams of the sun and the sightseers who invested their energy here gets enraptured by the regularly gleaming excellence of this pleasant land. It has a 600 km long shoreline specked with coconut forests, normal harbors, tidal ponds and shielded inlets. Kerala has probably the best slope stations in India with the whole Western Ghats studded with evergreens, moving prairies, sholas and stretches of reviving aroma of tea and espresso ranches. Table 2 shows the ar

Short Answers to Big Questions

Short Answers to Big Questions First, I have three very exciting pieces of news to share with you: 1) Googles homepage. 2) My favorite constellation is the APOD (Astronomy Picture Of the Day)!  According to the Greeks, the Pleides were the seven daughters (the constellation is also called The Seven Sisters) of Atlas and Pleione. To the best of my knowledge, no one really knows where the name Pleides came from, so it seems legitimate to pick the possibility that I like the most: plein means to sail, so the Pleides are sailing. Before you argue with that, go spend a few hours lying outside, and let yourself rotate under the stars. On a good night in Boston, I see an armless Orion, and the butt and tail of Ursa Major. One star of Casseiopia could represent the goddess knee, or her head. I like the Pleides because each star is an entire mythical person. The fourth brightest star, for example, is Maia: the oldest sailing sister. She gave birth to Hermes after being raped (surprise surprise) by Zeus. She is also, in case youre interested, a B8 III blue giant with a prominent mercury absorption line. Im sure each of Casseiopeias body parts has a story to tell, too, but there is a much higher density of mythological life stories in the Pleides than in any other part of the sky. My computer at the NRAO this summer was named maia; it felt like destiny. 3) It is beautiful outside. 76 ºF (24 ºC, for those of you who are like me) and cloudless. Its the kind of day that indulges every one of your senses. Now, to the actual content of this post. About a month ago, Chris e-mailed me about a Student Housing Panel. Apparently, there were a lot of new arrivals to the admissions office, and they needed to be brought up to speed about student life at MIT. Since I know a few things about being an MIT student, I was invited to sit on a panel and answer some questions. I had no idea what the questions were going to be. I imagined a fact request, like what is the housing process like for your dormitory? or what is the difference between 8.01 and 8.012? but instead had to improvise answers to (paraphrased): 1) What is your name / year / hometown / high school / major / residence? 2) Why did you choose MIT? 3) Whats your favorite thing about MIT? 4) Have you ever had a UROP? If so, what was the experience like? 5) Why did you choose your dorm/living group and how has it shaped you? 6) What are your biggest regrets from your years at MIT? 7) What activities are you involved with, and how have they shaped you? Admittedly, (1) was pretty straightforward, but the rest woah. Deep questions. Unfortunately I didnt have a notebook with me, so I whipped out a sheet of paper (this article, which my mom sent to me) and began to scribble on the back. When it was my turn to speak, responses came babbling out of me, although Im not sure what exactly I said. I just hadnt had to articulate answers to those questions before. Im glad someone forced me to: I think that theyre important ideas to have in my toolkit of Answers To Questions That Someone Might Ask Me Someday. Now that Ive had a little more time to reflect, here are more concise, confident answers. 1) Anna Ho. Class of 2014. Hometown: its complicated. I was born in Singapore, and moved to England when I was nine and a half, where I picked up an American accent. American School in London (hence the accent). Physics. French House, a living group in New House. 2) To be perfectly honest, I dont know. So, Ill speculate, the same way a historian might speculate about a subjects motivations, based on context and minimal historical records (I dont think I left anything in writing stating the reasons why.) I remember feeling conflicted, because I wanted to emerge from college a well-rounded individual; I was concerned that an MIT education would leave me humanities-less. I remember really admiring everyone I met from MIT, and admiring all of the bloggers on the admissions site. I wanted to be like them. I loved everyone I met during CPW, even though my tonsils rivalled golf balls in volume, and the person I spent the most time with over that weekend remains one of my best friends. I also remember perceiving a lack of pretention about MIT: no one seemed to care how you dressed, what color your hair was, where you came from, who your parents were, how athletic you were. Everyone just wanted to do, and talk about, interesting things. I remember hav ing a lot of respect for what people admired in each other: you would be praised for putting a car on the roof of a building, or for being really excited about your research, or for taking time out of your busy day to be a supportive friend. I remember a conversation back in London, with my writing seminar teacher; when I told him that I was considering going to MIT, he said: oh, MIT! They have a great writing department! Did you know that? Ultimately, I think I picked MIT because, after reading about past MIT students for years (since 8th grade) and meeting current and future ones, I decided that I wanted to be an MIT student. I wanted to be good at the things MIT students admired each other for. I looked up to every individual on that campus, and maybe that made me think going there would turn me into the best person I could be. But thats just an educated guess. Another possibility is that I just made a gut instinct decision. And thats worked out fine! 3) The answer almost everyone gives is the people, so Im going to talk about a couple of other things. The energy. You walk down the hallway, and everyone is walking quickly, with purpose. You catch snippets of excited conversations about projects and stories and wish you had time to listen to all of them. MIT changes us. During orientation, I meet freshmen who are just off the boat from high school, where their identity was The Smart Kid. They are keen to impress. They arrive, and insecurity floods in: everyone around you is OUTSTANDING so you feel very ordinary, and scramble to become distinct. At first, you dont know how you want to distinguish yourself. You talk loudly about a pset score, or about how late you were up studying, or jump to correct people on little insignificant techncialities (spoiler alert: none of these things are particularly impressive.) For some reason, it took me a while to get that admiring others and feeling proud of myself are NOT mutually exclusive. It took me a while to learn that I stand out in ways independent of where I would fall on an IQ or GPA spectrum. Ive learned, for example, that I am very good at infecting others with my excitement for a topic, and that I have a knack for public speaking. One of my friends, on the other hand, is not fond of public speaking at all, yet has incredible to-die-for self-discipline. She exercises all the time, does her grocery shopping regularly (WOW), eats very healthily (WOW), and sleeps well. Ive seen her study for a test every day for a week, or every week for months. I would never say that shes the smartest person I know, but Ive also learned that thats a meaningless compliment, when everyone is intelligence in such a vast array of ways. I was very attached to The Smart Kid title in High School (its addictive) and being stripped of that title on MIT campus can be a p ainful, painful process. But here, Ive had the incentive the need, really to distinguish myself in healthier, more productive ways, and I think that thats made me much better-equipped to enter the world. I also like how much innate respect MIT students have for each other. When I meet someone, I assume that he or she is very competent, kind, and has my best interests at heart. I know that this person has pursued passions in an exceptional way or, frankly, they wouldnt be here and I am excited right off the bat to learn what that story is. I like how much responsibility MIT students take for and give to each other. The spirit here is that were all very intelligent competent people, who care very much about our unique campus culture, and therefore we want a big say in administrative changes. We have a HUGE role in managing our housing system: within our dorms, we basically run CPW and FYRE  and  rooming lotteries. In French House, we even feed each other, through our daily (minus Saturday) cooking system. We take care of each other, here. 4) Yes, and mixed. My first UROP was freshman year; I worked in Saxelab, after introducing myself to the PI following a BCS colloquium. I interviewed for the position, then worked with two post-docs for a few months on a project studying the eye movements of autistic subjects while they watch complex social scenes. It was totally fascinating in theory, but the day-to-day work was tedious; I combed through videos, trying to find appropriate scenes for the study. I didnt learn a whole lot about the brain. In retrospect, I wish I had started the project over IAP or over the summer, so that I could have devoted more time to it. Exposure to the lab did give me a sense for what behavioral study work is like, though, and I learned that I wanted to try something else. Next up: summer after freshman year, I did a computational biology-esque UROP with a grad student in the mechanical engineering department (he was quite the polymath.) Again, that was really interesting but I didnt click particularly well with the mentor and in the end it didnt really go anywhere. So, again, another good learning experience, but meh. Everything changed when I did an REU that I absolutely loved. This was really my transformative research experience for some people, that takes place through a UROP on campus instead. 5) The how it has shaped me is much easier than the why I picked it. How I ended up living here isnt a very romantic story. I didnt get much of a chance to explore the dorms: I was sick with tonsillitis during CPW, and on crutches during REX. I had studied French all my life and had spent a lot of time in France, so was definitely drawn to the cultural aspect, without really knowing what I was in for. Either way, somehow I ended up here, and really could not be happier about it! Now: how its shaped me. At home, my major responsibility was to myself: work hard and develop a set of interests, while Mom and Dad take care of necessities. I stayed far away from student government activities, although I did run a few clubs. My robotics team was probably where I developed my strongest sense of responsibility for others, but at the same time there were always adult mentors who REALLY ran things: organized trips, encouraged us to go out and find funding, etc. French House runs itself. We manage our own budget, debate at house meetings how and when to spend our money. We buy our own kitchen equipment, cook meals for each other, split up the cleaning chores. We plan, organize, run freshmen orientation activities, and ditto social events like dinners and parties. In French House, Ive learned how to feel responsible for my family: things literally would not happen here we would not have dinners, we would not have kitchen equipment, our living space would not be clean if we stopped taking care of it, and each other. Almost all of the upperclassman members of the house have some kind of house government position: this year, Im an orientation chair and sports chair, for example. Im glad that I didnt pick a living group by trying to find the group of people most similar to me.  If I did, I wouldnt have ended up in French House. Sure, its important to live with people you feel comfortable with, but learning to live with people who are different from you is also important and something you will rarely have the opportunity to do, after college. We have a huge diversity of residents here: a range of majors, interests, hobbies, habits, personality types, and as a result, Ive been inspired in ways that I would otherwise never have been, and become best friends with people I would otherwise never have met.   6) Regrets. This is a really hard question, because any regret can be cast as an important life lesson. I do regret not holding onto more my friendships: there are people I talked to a lot freshmen year, who I now wave to in the infinite every now and then. I regret not making a point to exercise regularly. Fortunately, the long walk to New House and the hike up the stairs to French House has kept me reasonably in-shape, but I wish I had made a point of establishing an exercise habit. Other than that, I cant think of anything I really wish I had or hadnt done: I definitely made a lot of mistakes, but I think they all needed to be made. 7) This could be a novella. I wont provide a laundry list. Instead, Ill focus on two that have had totally unexpected but transforming outcomes: -Musical Theater. Ive performed in two musicals at MIT, and the performers confidence Ive gained as a result has made me a MUCH better teacher and public speaker. These are skills that Ive used since to give talks on my research to the public, an activity that ultimately shifted my career path from doctor to astrophysicist public outreach-er. -Dorm Government. I stayed far, far away from dorm government during High School. I sort of just didnt want to know, I think, and felt like I had better things to do. Here at MIT, Ive gotten very heavily involved with politics: Im the president of my dorm, serve as a student rep to the CUP, and have developed a very strong feeling of responsibility for my community as a result. Ive been through some rough patches, but have become so much more adept at navigating the waters of decision-making and consulting and knowing when to ask for advice and when to just make a decision. My spine is much tougher, Ive learned to stand up and fight, how to respond to emergencies. Ive also gotten to know a much wider cross-section of the campus community. Ive learned that at the end of the day, were all MIT students, and which dorm we live in should not limit the radius of our circle of friendships. Its been stressful, not going to lie but a total privilege, and Im now much more aware of my personal strengths and weaknesses.. And hopefully a much better leader. After my term is over, and I have more time to reflect on the experience as a closed system, Ill write a more detailed post about it. When the panel was over, my head was left buzzing with how much of a roller-coaster college has been. What an amazingly high density of learning and changing we do in these four years. And what a weird feeling, to think that I will bow out of this universe in under two semesters.

1 Student 1 Sport Policy - 1750 Words

1Student 1Sport Policy (1M 1S) Sports should be integral to a person’s life. This is due to the benefits in health that can be derived from it and also skills such as strategic thinking and teamwork can be learnt. Most pupils have benefitted from participation in various sports, but most voluntarily participated in the sport activities of their choice. Sports serve as an excellent physical exercise. Those who play sports have a more positive body image than those who do not. Sports often involve physical activities like running, jumping, stretching and moving about which turn out to be a good body workout. Playing sports is energy put to good use. A co-curricular activity is defined as a program or out-of-class activity, supervised and or†¦show more content†¦It is assured that academic results would not be affected, instead making the students all-rounders. â€Å"Any effects on sports participants will be determined by the frequency of participation, intensity of participation, and their degree of adherence over time. Although these factors are especially important in order to obtain fitness and health benefits, they also have implications for the development of sporting and social skills and changed attitudes and values.†(Professor Fred Coalter, Institute for Sports Research University of Stirling, (January,2005) Playing sports is very beneficial for the development of social skills. Sports teach you to interact with people, communicate with them and collaborate as a team. Sports foster collective thinking and harness your planning and delegation skills too. Sports build confidence. Winning a game gives you a sense of accomplishment, which boosts your confidence further. Participation in sports can have a major effect on children in the classroom as well. Children who are involved in sports often develop time management skills that are helpful with academic studies. Many schools promote the link between sports and academia by establishing minimum grade requirements that must be met in order to participate in sports. â€Å"Research shows that sports improve Math skills in children. Sports that involve aiming and hitting skills, for example, tennis, badminton, baseball and cricket help them increase focus.Show MoreRelatedShould Club Sports Be Competitive Sports?1148 Words   |  5 PagesParticipation in college club sports continues to rise with an estimated two million students currently involved. These clubs provide an attractive alternative for students who wish to continue competitive sports without the time commitment associated with intercollegiate athletics. 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The Nature of Perceived Ultimacy in Zen Buddhism Essay

This paper will explore the question of how to understand the nature of perceived ultimacy in Zen Buddhism. This will be achieved through providing a justification for why this question should be of any interest and then hypothesizing about possible implications of the results. Next, the framework that is to be used in categorizing the core beliefs in Zen will be explained and made clear. After this description is complete the author will proceed to fit Zen Buddhism into this framework and will demonstrate that the Zen religion is no exception to the employed framework. Finally the author will describe the perceived ultimacy of Zen Buddhism. The topic of Zen Buddhism and understanding how it fits into a framework that was designed to†¦show more content†¦Even when we are presented with answers or guides to the many questions we have about life and to how we should live, as inquisitive animals, we strive to enhance our understanding and so begin to learn that perhaps, ultimately, the answers don’t simply come from outside but also from within us. This is then perhaps the greatest implication of this paper, finding new ways in understanding what the true way of life is for human beings and what the true way of life is for ourselves. In the discussion of Zen Buddhism, William A. Young’s framework’s itself must first be explained and understood. Young employs a descriptive framework in his book The World’s Religions that is used to understand religion and the ways in which religion plays various roles in human life (Young 12). The framework was developed from the definition of religion he describes in his book. Young defines religion as being, â€Å"human transformation in response to perceived ultimacy† (4). This framework developed by Young was a tool of analysis he employed to compare religions through seven questions that formulate a basic understanding of a particular religion’s worldview. The seven questions that make up Young’s framework are as follows: what does it mean to be human, what is the basic human problem, what is the cause of the problem, what is the end or goal of transformation, what are the means of transformation, what is the nature of reality, and what

Cell and Molecular Biology Free Essays

Cell and Molecular Biology Final Name: Hadeel Binomar30 pts. Protein misfolding can be an aspect of several different human disorders, including cystic fibrosis, Alzheimer’s disease, and atherosclerosis. Many times, the misfolded protein is a membrane protein. We will write a custom essay sample on Cell and Molecular Biology or any similar topic only for you Order Now In fact, a type of diabetes insipidus results from a mutation in the G-protein-coupled vasopressin 2 receptor that prevents the protein from making it to the cell membrane A) Describe how this type of receptor would normally get targeted to the membrane (from the beginning of translation) and B) then propose one mechanism by which the mutation could cause a lack of proper targeting. One of the most important protein’s target is G protein-coupled receptors, several signaling mechanisms depend on this type of receptor to change both internal and external stimuli to the intracellular responses. Basically, one of the G couple receptor subfamilies is G-coupled Vasopressin-2- Receptor (V2R), and this receptor is going through a strict quality control process at the endoplasmic reticulum, which presents the only correctly folded protein to gets through the secretory pathway. The primary function of the V2 receptor is to activate the attached G protein that bound to the ? subunit then phosphorylated to GTP. The G protein couple receptor then activates the enzyme adenylate cyclase that catalyzes the reaction in the ER and forms cAMP from ATP. After that, cAMP acts as a second messenger and activates a protein kinase that phosphorylates the integral membrane proteins on the cell surface. Moreover, the secretory pathway organelles’ and the plasma membrane both are first introduced into the Endoplasmic reticulum, and the co-translationally proteins that can cross the ER are synthesized by the ribosome first then binds by chaperones to gets moves to the ER surface using GTP that allows them to move toward the receptor then release it. The soluble proteins and the integral membrane proteins as I mentioned above, can be targeted through the ER and then translocated by the same mechanism.Further, several mutations occurring in the transmembrane region which affect the structure of the protein. These are multiple mutation sites, such as mutations occurring in the amino acid residues which was acting as a causative agent for human disease. Also, there are other mutations occurring on the single site position that will affect the translation mechanism and cause many human diseases like: cystic fibrosis, Alzheimer’s disease, and atherosclerosis that proves the function of V2R protein which plays important role in the translation during the protein folding process. One of the mechanism that may a reason for lacking the proper target protein is when the mutations of the CFTR gene occurring and affect the function of the chloride ion channels and cause defect in the protein sequences which lead to the production of diseases and misfolded of the proteins that are unable to recognize their functional destinations. Otherwise, Lack of the stop signals is another issue that prevents the protein from getting into the surface of the ER, also called the non-stop decay cellular pathway, because lack of this stop signals prevents mRNA from synthesis and translate the proteins, these consider as a point mutation that inhibits the essential stop codons. 30 pts. Describe the experiment shown in figure 3 from the paper we discussed in class (Miller et al, 2003). (A) In your description, consider the following questions: Why did they do it? How did they do it? What did they learn? (B) Diagram the results that you would expect to see in Lanes T, 1, 2, 3, and 4, if the amino acid signal DID in the protein Gap1p was mutated to random amino acids and tell why; and (C) Give two possible (different) results that might occur if the amino acid signal LxxLE in Bet1p was mutated to the amino acids DID (which are the signal in Gap1p). Diagram the results expected in Lanes T, 1, 2, 3, and 4 and explain why you predicted this result for each case.left20840701.A001.A4467225201739500The experiment was performed to study the role of cargo binding domain of Sec24p in the process of protein sorting. To perform this study, both mutant and wild types subunit Sec23/24p and Sec23/24L616W were harvested from microsomal membranes. The immunoblotting assay performed to quantify cargo molecules using radio-labeled secondary antibodies. Comparison of the mutant subunit with wild type illustrated omission of some molecules in mutant one, these molecules were cargo protein molecules. While some of them are packed in a way that similar to the wild-type. It meant that there were some signals that remained unaffected although mutation was there. Unexpectedly, it was found that in these unaffected molecules of mutation in Sec23/24p, packaging was better than the wild type. Further, they found the proteins that were highly affected had Bet1p and Gap1p/Sys1p chimera, because they completely depending on the Sys1p di-acidic of COPII vesicles. If the amino acid signal DID in the protein Gap1p was mutated to random amino acids, the resulting bands would be seen as in figure 1. A because the amino acids might be present in all the lanes. And Gap1p is required for di-acidic motifs to fuse together with the COPII vesicles at the mutated domain. Also, Sys1 peptide is not involved in Sec 23/24p hence its mutation is not contained in a di-acidic motif. If the signal LxxLE was mutated to the DID, the expected Bet1p packaging would be shown in figure 2. A as not be seen in lanes containing Bet1p because the amino acid signal LxxLE does not exit after mutating to amino acids DID. The second probability for the Bet1p would be expected to bind with the vesicle for packaging when it interacts with di-acidic motifs which is needed as shown in figure 2.B290512515621000581025113030004781550412752.B002.B6286501346202.A002.A20 pts. Explain the experiment shown in Figure 5C from the Shen et al. (2018) paper on the phosphorylation of CDC25 that we discussed in class. In addition, be sure to also address the following: A) why did they do this experiment (the central issue); B) what did they learn; and C) what is another control experiment they could have done? D) Would these results change if you added a constitutively active form of LKB1 to the reaction? If so, how and why? A) Overall, the main purpose of this paper is to explain how the division of cells is highly regulated such that cells that fail to pass some specific stage-based tests cannot advance to the proceeding stages. In this particular experiment, HeLa cells were subjected to chemicals that are known to activate the enzyme AMPK. Also, the main catabolic processes that are involved to generate energy for cells to transition from G1/G2 were determined by the application of radiochemical approaches, the experiment required to approve how highly conserved cellular energy sensor can significantly delay mitosis entry and activation of AMP-activated protein kinase (AMPK). Further, Wee 1 family inactivates the cell cycle G2/M Phase which is controlled by Cdc3/cyclic B (mitotic cyclin-dependent kinase complex). They found that AMPK-dependents phosphorylation of CDC25C arranges a metabolic control point for the M-phase transition and the cell cycle phase G2. B) Also, they learned that suppression of Wee 1 or acute induction partially reinstates mitosis ingress in the circumstance of activated protein kinase (AMPK). This experiment showed that when Phosphorylates Cdc25 is in a distributive and disordered state, it results into ultra-sensitivity in protein phosphorylation. C) For another control experiment, they might try exposing the U2OS (cell line) clones conditionally exhibiting Cdc25A etoposide. That will help to test whether Cdc25A degradation is significant for the G2 control point or not.D) If they add an active form of LKB1 to the reaction, the results will not change, because in cells LKBI activity inhibits AMPK activation in response to different stimulations. Also, LKBI is lost upon consistent isolation and therefore no effects of phosphates observed.20 pts. Briefly describe the role of cyclin-CDK in the cell cycle and give an example of positive and negative control in this system. Also, describe how cell cycle regulation links to the stimulation of apoptosis at the molecular level. In the beginning, the cell cycle depends on many basic factors that control the regulation process starting from the signal transcription molecules, growth factors and the Cyclin Dependent Kinases enzymes include the checkpoints which control the transition process between the cell cycle phases by binding to the cyclin proteins CDKs then phosphorylate other proteins to transfer from one phase to another. The role of transcription factors is to turn on the signals for gene expression, DNA replication, and cell divisions. As an example of CDKs, cyclin-dependent kinase 1 CDK1 is a cell division cycle protein homolog 2, that has a primary role in human cancer cells because CDK1 rather than any types of CDKs is fatal to the mutated version of MYC- dependent cancer that leads to a depletion of oncogenes like (Fos and Jun) in human cancer cells. Fos and Jun are combined forms of the transcription factor called AP1 that activates the delayed response genes such as cyclin D and CDK4. Recent studies reveal that the reason for the MYC breast cancer cells duplation is targeting CDF1 exhibit any other CDKs cell lines. Also, CDK1 inhibition can control and target the cancer cells in human and both phosphorylation and expression of MYC during the cell cycle process. To initiate intracellular signaling pathways and stimulate the cell cycle entry, mitogens substance bind to the cell surface receptor with the activation form of GTPase Ras that activates MAP kinase cascade. That will lead to the expression of encoding gene of the transcription regulatory protein like MYC. Moreover, E2F transcription factor is a target for cyclin D and CDKs that stimulate proteins expression to initiate S phase, also E2F regulated by the tumor suppressor gene Rb (Retinoblastoma protein). At early G1 Phase, Rb protein combined with E2f to form the histone deacetylases protein that remains chromatic condensed, then cyclin kinase phosphorylates Rb protein, causing it to disassociate from E2F. That allows recruitment of histone acetylates, which decondense the chromatin and helps transcription complexes to form in G1 and S phase and to form a positive feedback. For the negative control, if there are no growth factors present to stimulate the synthesis of Cyclin D in the new cell, Rb phosphorylated will turn off, and Rb will rebind to E2F, then the cell cycle will stop and that will lead to many negative results like prevent it to bind with DNA, or DNA damage and cells will return to the G0 phase. Apoptosis is a consequence of DNA damage; if the damage is not repaired, the cell cycle will divert towards apoptosis, otherwise, if the cell has DNA defects and fail to undergo apoptosis, that will change to the cancer cell. G1 phase regulators such as P53 and E2F are essential to promote the cell regulations and eliminate any damage or abnormal changes during the cell cycle. P53 has a primary function to prevent any mutation in DNA during cell progression, so any defect in P53 will lead to cancer, and it’s usually mutated in cancer cells. Further, Rb protein considers as a tumor suppressor and also promotes apoptosis. Additionally, most human cancers have inactive Rb protein, either mutated Rb or the non-phosphorylated (inactivated form) of Rb protein How to cite Cell and Molecular Biology, Papers

Cell and Molecular Biology Free Essays

Cell and Molecular Biology Final Name: Hadeel Binomar30 pts. Protein misfolding can be an aspect of several different human disorders, including cystic fibrosis, Alzheimer’s disease, and atherosclerosis. Many times, the misfolded protein is a membrane protein. We will write a custom essay sample on Cell and Molecular Biology or any similar topic only for you Order Now In fact, a type of diabetes insipidus results from a mutation in the G-protein-coupled vasopressin 2 receptor that prevents the protein from making it to the cell membrane A) Describe how this type of receptor would normally get targeted to the membrane (from the beginning of translation) and B) then propose one mechanism by which the mutation could cause a lack of proper targeting. One of the most important protein’s target is G protein-coupled receptors, several signaling mechanisms depend on this type of receptor to change both internal and external stimuli to the intracellular responses. Basically, one of the G couple receptor subfamilies is G-coupled Vasopressin-2- Receptor (V2R), and this receptor is going through a strict quality control process at the endoplasmic reticulum, which presents the only correctly folded protein to gets through the secretory pathway. The primary function of the V2 receptor is to activate the attached G protein that bound to the ? subunit then phosphorylated to GTP. The G protein couple receptor then activates the enzyme adenylate cyclase that catalyzes the reaction in the ER and forms cAMP from ATP. After that, cAMP acts as a second messenger and activates a protein kinase that phosphorylates the integral membrane proteins on the cell surface. Moreover, the secretory pathway organelles’ and the plasma membrane both are first introduced into the Endoplasmic reticulum, and the co-translationally proteins that can cross the ER are synthesized by the ribosome first then binds by chaperones to gets moves to the ER surface using GTP that allows them to move toward the receptor then release it. The soluble proteins and the integral membrane proteins as I mentioned above, can be targeted through the ER and then translocated by the same mechanism.Further, several mutations occurring in the transmembrane region which affect the structure of the protein. These are multiple mutation sites, such as mutations occurring in the amino acid residues which was acting as a causative agent for human disease. Also, there are other mutations occurring on the single site position that will affect the translation mechanism and cause many human diseases like: cystic fibrosis, Alzheimer’s disease, and atherosclerosis that proves the function of V2R protein which plays important role in the translation during the protein folding process. One of the mechanism that may a reason for lacking the proper target protein is when the mutations of the CFTR gene occurring and affect the function of the chloride ion channels and cause defect in the protein sequences which lead to the production of diseases and misfolded of the proteins that are unable to recognize their functional destinations. Otherwise, Lack of the stop signals is another issue that prevents the protein from getting into the surface of the ER, also called the non-stop decay cellular pathway, because lack of this stop signals prevents mRNA from synthesis and translate the proteins, these consider as a point mutation that inhibits the essential stop codons. 30 pts. Describe the experiment shown in figure 3 from the paper we discussed in class (Miller et al, 2003). (A) In your description, consider the following questions: Why did they do it? How did they do it? What did they learn? (B) Diagram the results that you would expect to see in Lanes T, 1, 2, 3, and 4, if the amino acid signal DID in the protein Gap1p was mutated to random amino acids and tell why; and (C) Give two possible (different) results that might occur if the amino acid signal LxxLE in Bet1p was mutated to the amino acids DID (which are the signal in Gap1p). Diagram the results expected in Lanes T, 1, 2, 3, and 4 and explain why you predicted this result for each case.left20840701.A001.A4467225201739500The experiment was performed to study the role of cargo binding domain of Sec24p in the process of protein sorting. To perform this study, both mutant and wild types subunit Sec23/24p and Sec23/24L616W were harvested from microsomal membranes. The immunoblotting assay performed to quantify cargo molecules using radio-labeled secondary antibodies. Comparison of the mutant subunit with wild type illustrated omission of some molecules in mutant one, these molecules were cargo protein molecules. While some of them are packed in a way that similar to the wild-type. It meant that there were some signals that remained unaffected although mutation was there. Unexpectedly, it was found that in these unaffected molecules of mutation in Sec23/24p, packaging was better than the wild type. Further, they found the proteins that were highly affected had Bet1p and Gap1p/Sys1p chimera, because they completely depending on the Sys1p di-acidic of COPII vesicles. If the amino acid signal DID in the protein Gap1p was mutated to random amino acids, the resulting bands would be seen as in figure 1. A because the amino acids might be present in all the lanes. And Gap1p is required for di-acidic motifs to fuse together with the COPII vesicles at the mutated domain. Also, Sys1 peptide is not involved in Sec 23/24p hence its mutation is not contained in a di-acidic motif. If the signal LxxLE was mutated to the DID, the expected Bet1p packaging would be shown in figure 2. A as not be seen in lanes containing Bet1p because the amino acid signal LxxLE does not exit after mutating to amino acids DID. The second probability for the Bet1p would be expected to bind with the vesicle for packaging when it interacts with di-acidic motifs which is needed as shown in figure 2.B290512515621000581025113030004781550412752.B002.B6286501346202.A002.A20 pts. Explain the experiment shown in Figure 5C from the Shen et al. (2018) paper on the phosphorylation of CDC25 that we discussed in class. In addition, be sure to also address the following: A) why did they do this experiment (the central issue); B) what did they learn; and C) what is another control experiment they could have done? D) Would these results change if you added a constitutively active form of LKB1 to the reaction? If so, how and why? A) Overall, the main purpose of this paper is to explain how the division of cells is highly regulated such that cells that fail to pass some specific stage-based tests cannot advance to the proceeding stages. In this particular experiment, HeLa cells were subjected to chemicals that are known to activate the enzyme AMPK. Also, the main catabolic processes that are involved to generate energy for cells to transition from G1/G2 were determined by the application of radiochemical approaches, the experiment required to approve how highly conserved cellular energy sensor can significantly delay mitosis entry and activation of AMP-activated protein kinase (AMPK). Further, Wee 1 family inactivates the cell cycle G2/M Phase which is controlled by Cdc3/cyclic B (mitotic cyclin-dependent kinase complex). They found that AMPK-dependents phosphorylation of CDC25C arranges a metabolic control point for the M-phase transition and the cell cycle phase G2. B) Also, they learned that suppression of Wee 1 or acute induction partially reinstates mitosis ingress in the circumstance of activated protein kinase (AMPK). This experiment showed that when Phosphorylates Cdc25 is in a distributive and disordered state, it results into ultra-sensitivity in protein phosphorylation. C) For another control experiment, they might try exposing the U2OS (cell line) clones conditionally exhibiting Cdc25A etoposide. That will help to test whether Cdc25A degradation is significant for the G2 control point or not.D) If they add an active form of LKB1 to the reaction, the results will not change, because in cells LKBI activity inhibits AMPK activation in response to different stimulations. Also, LKBI is lost upon consistent isolation and therefore no effects of phosphates observed.20 pts. Briefly describe the role of cyclin-CDK in the cell cycle and give an example of positive and negative control in this system. Also, describe how cell cycle regulation links to the stimulation of apoptosis at the molecular level. In the beginning, the cell cycle depends on many basic factors that control the regulation process starting from the signal transcription molecules, growth factors and the Cyclin Dependent Kinases enzymes include the checkpoints which control the transition process between the cell cycle phases by binding to the cyclin proteins CDKs then phosphorylate other proteins to transfer from one phase to another. The role of transcription factors is to turn on the signals for gene expression, DNA replication, and cell divisions. As an example of CDKs, cyclin-dependent kinase 1 CDK1 is a cell division cycle protein homolog 2, that has a primary role in human cancer cells because CDK1 rather than any types of CDKs is fatal to the mutated version of MYC- dependent cancer that leads to a depletion of oncogenes like (Fos and Jun) in human cancer cells. Fos and Jun are combined forms of the transcription factor called AP1 that activates the delayed response genes such as cyclin D and CDK4. Recent studies reveal that the reason for the MYC breast cancer cells duplation is targeting CDF1 exhibit any other CDKs cell lines. Also, CDK1 inhibition can control and target the cancer cells in human and both phosphorylation and expression of MYC during the cell cycle process. To initiate intracellular signaling pathways and stimulate the cell cycle entry, mitogens substance bind to the cell surface receptor with the activation form of GTPase Ras that activates MAP kinase cascade. That will lead to the expression of encoding gene of the transcription regulatory protein like MYC. Moreover, E2F transcription factor is a target for cyclin D and CDKs that stimulate proteins expression to initiate S phase, also E2F regulated by the tumor suppressor gene Rb (Retinoblastoma protein). At early G1 Phase, Rb protein combined with E2f to form the histone deacetylases protein that remains chromatic condensed, then cyclin kinase phosphorylates Rb protein, causing it to disassociate from E2F. That allows recruitment of histone acetylates, which decondense the chromatin and helps transcription complexes to form in G1 and S phase and to form a positive feedback. For the negative control, if there are no growth factors present to stimulate the synthesis of Cyclin D in the new cell, Rb phosphorylated will turn off, and Rb will rebind to E2F, then the cell cycle will stop and that will lead to many negative results like prevent it to bind with DNA, or DNA damage and cells will return to the G0 phase. Apoptosis is a consequence of DNA damage; if the damage is not repaired, the cell cycle will divert towards apoptosis, otherwise, if the cell has DNA defects and fail to undergo apoptosis, that will change to the cancer cell. G1 phase regulators such as P53 and E2F are essential to promote the cell regulations and eliminate any damage or abnormal changes during the cell cycle. P53 has a primary function to prevent any mutation in DNA during cell progression, so any defect in P53 will lead to cancer, and it’s usually mutated in cancer cells. Further, Rb protein considers as a tumor suppressor and also promotes apoptosis. Additionally, most human cancers have inactive Rb protein, either mutated Rb or the non-phosphorylated (inactivated form) of Rb protein How to cite Cell and Molecular Biology, Papers