1. Which chemical is the most common photographic fixer

Answer: Hypo

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MCQ-> Cells are the ultimate multi-taskers: they can switch on genes and carry out their orders, talk to each other, divide in two, and much more, all at the same time. But they couldn’t do any of these tricks without a power source to generate movement. The inside of a cell bustles with more traffic than Delhi roads, and, like all vehicles, the cell’s moving parts need engines. Physicists and biologists have looked ‘under the hood’ of the cell and laid out the nuts and bolts of molecular engines.The ability of such engines to convert chemical energy into motion is the envy nanotechnology researchers looking for ways to power molecule-sized devices. Medical researchers also want to understand how these engines work. Because these molecules are essential for cell division, scientists hope to shut down the rampant growth of cancer cells by deactivating certain motors. Improving motor-driven transport in nerve cells may also be helpful for treating diseases such as Alzheimer’s, Parkinson’s or ALS, also known as Lou Gehrig’s disease.We wouldn’t make it far in life without motor proteins. Our muscles wouldn’t contract. We couldn’t grow, because the growth process requires cells to duplicate their machinery and pull the copies apart. And our genes would be silent without the services of messenger RNA, which carries genetic instructions over to the cell’s protein-making factories. The movements that make these cellular activities possible occur along a complex network of threadlike fibers, or polymers, along which bundles of molecules travel like trams. The engines that power the cell’s freight are three families of proteins, called myosin, kinesin and dynein. For fuel, these proteins burn molecules of ATP, which cells make when they break down the carbohydrates and fats from the foods we eat. The energy from burning ATP causes changes in the proteins’ shape that allow them to heave themselves along the polymer track. The results are impressive: In one second, these molecules can travel between 50 and 100 times their own diameter. If a car with a five-foot-wide engine were as efficient, it would travel 170 to 340 kilometres per hour.Ronald Vale, a researcher at the Howard Hughes Medical Institute and the University of California at San Francisco, and Ronald Milligan of the Scripps Research Institute have realized a long-awaited goal by reconstructing the process by which myosin and kinesin move, almost down to the atom. The dynein motor, on the other hand, is still poorly understood. Myosin molecules, best known for their role in muscle contraction, form chains that lie between filaments of another protein called actin. Each myosin molecule has a tiny head that pokes out from the chain like oars from a canoe. Just as rowers propel their boat by stroking their oars through the water, the myosin molecules stick their heads into the actin and hoist themselves forward along the filament. While myosin moves along in short strokes, its cousin kinesin walks steadily along a different type of filament called a microtubule. Instead of using a projecting head as a lever, kinesin walks on two ‘legs’. Based on these differences, researchers used to think that myosin and kinesin were virtually unrelated. But newly discovered similarities in the motors’ ATP-processing machinery now suggest that they share a common ancestor — molecule. At this point, scientists can only speculate as to what type of primitive cell-like structure this ancestor occupied as it learned to burn ATP and use the energy to change shape. “We’ll never really know, because we can’t dig up the remains of ancient proteins, but that was probably a big evolutionary leap,” says Vale.On a slightly larger scale, loner cells like sperm or infectious bacteria are prime movers that resolutely push their way through to other cells. As L. Mahadevan and Paul Matsudaira of the Massachusetts Institute of Technology explain, the engines in this case are springs or ratchets that are clusters of molecules, rather than single proteins like myosin and kinesin. Researchers don’t yet fully understand these engines’ fueling process or the details of how they move, but the result is a force to be reckoned with. For example, one such engine is a spring-like stalk connecting a single-celled organism called a vorticellid to the leaf fragment it calls home. When exposed to calcium, the spring contracts, yanking the vorticellid down at speeds approaching three inches (eight centimetres) per second.Springs like this are coiled bundles of filaments that expand or contract in response to chemical cues. A wave of positively charged calcium ions, for example, neutralizes the negative charges that keep the filaments extended. Some sperm use spring-like engines made of actin filaments to shoot out a barb that penetrates the layers that surround an egg. And certain viruses use a similar apparatus to shoot their DNA into the host’s cell. Ratchets are also useful for moving whole cells, including some other sperm and pathogens. These engines are filaments that simply grow at one end, attracting chemical building blocks from nearby. Because the other end is anchored in place, the growing end pushes against any barrier that gets in its way.Both springs and ratchets are made up of small units that each move just slightly, but collectively produce a powerful movement. Ultimately, Mahadevan and Matsudaira hope to better understand just how these particles create an effect that seems to be so much more than the sum of its parts. Might such an understanding provide inspiration for ways to power artificial nano-sized devices in the future? “The short answer is absolutely,” says Mahadevan. “Biology has had a lot more time to evolve enormous richness in design for different organisms. Hopefully, studying these structures will not only improve our understanding of the biological world, it will also enable us to copy them, take apart their components and recreate them for other purpose.”According to the author, research on the power source of movement in cells can contribute to
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MCQ-> Throughout human history the leading causes of death have been infection and trauma, Modem medicine has scored significant victories against both, and the major causes of ill health and death are now the chronic degenerative diseases, such as coronary artery disease, arthritis, osteoporosis, Alzheimer’s, macular degeneration, cataract and cancer. These have a long latency period before symptoms appear and a diagnosis is made. It follows that the majority of apparently healthy people are pre-ill.But are these conditions inevitably degenerative? A truly preventive medicine that focused on the pre-ill, analyzing the metabolic errors which lead to clinical illness, might be able to correct them before the first symptom. Genetic risk factors are known for all the chronic degenerative diseases, and are important to the individuals who possess them. At the population level, however, migration studies confirm that these illnesses are linked for the most part to lifestyle factors — exercise, smoking and nutrition. Nutrition is the easiest of these to change, and the most versatile tool for affecting the metabolic changes needed to tilt the balance away from disease.Many national surveys reveal that malnutrition is common in developed countries. This is not the calorie and/or micronutrient deficiency associated with developing nations (type A malnutrition); but multiple micronutrient depletion, usually combined with calorific balance or excess (Type B malnutrition). The incidence and severity of Type B malnutrition will be shown to be worse if newer micronutrient groups such as the essential fatty acids, xanthophylls and falconoid are included in the surveys. Commonly ingested levels of these micronutrients seem to be far too low in many developed countries.There is now considerable evidence that Type B malnutrition is a major cause of chronic degenerative diseases. If this is the case, then t is logical to treat such diseases not with drugs but with multiple micronutrient repletion, or pharmaco-nutrition’. This can take the form of pills and capsules — ‘nutraceuticals’, or food formats known as ‘functional foods’, This approach has been neglected hitherto because it is relatively unprofitable for drug companies — the products are hard to patent — and it is a strategy which does not sit easily with modem medical interventionism. Over the last 100 years, the drug industry has invested huge sums in developing a range of subtle and powerful drugs to treat the many diseases we are subject to. Medical training is couched in pharmaceutical terms and this approach has provided us with an exceptional range of therapeutic tools in the treatment of disease and in acute medical emergencies. However, the pharmaceutical model has also created an unhealthy dependency culture, in which relatively few of us accept responsibility for maintaining our own health. Instead, we have handed over this responsibility to health professionals who know very little about health maintenance, or disease prevention.One problem for supporters of this argument is lack of the right kind of hard evidence. We have a wealth of epidemiological data linking dietary factors to health profiles/ disease risks, and a great deal of information on mechanism: how food factors interact with our biochemistry. But almost all intervention studies with micronutrients, with the notable exception of the omega 3 fatty acids, have so far produced conflicting or negative results. In other words, our science appears to have no predictive value. Does this invalidate the science? Or are we simply asking the wrong questions?Based on pharmaceutical thinking, most intervention studies have attempted to measure the impact of a single micronutrient on the incidence of disease. The classical approach says that if you give a compound formula to test subjects and obtain positive results, you cannot know which ingredient is exerting the benefit, so you must test each ingredient individually. But in the field of nutrition, this does not work. Each intervention on its own will hardly make enough difference to be measured. The best therapeutic response must therefore combine micronutrients to normalise our internal physiology. So do we need to analyse each individual’s nutritional status and then tailor a formula specifically for him or her? While we do not have the resources to analyze millions of individual cases, there is no need to do so. The vast majority of people are consuming suboptimal amounts of most micronutrients, and most of the micronutrients concerned are very safe. Accordingly, a comprehensive and universal program of micronutrient support is probably the most cost-effective and safest way of improving the general health of the nation.The author recommends micronutrient-repletion for large-scale treatment of chronic degenerative diseases because
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