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Tuesday, July 7, 2015

Tesla Is Betting on Solar, Not Just Batteries 07-07


Tesla Is Betting on Solar, Not Just Batteries





















Tesla’s Powerwall storage system is not a radical innovation, and it is not the first battery for energy storage on the market. But, as Elon Musk surely understands, it is not always the best technology that wins the innovation race. Rather, it’s often the one that best fits with existing dominant technologies, so that the success of the two becomes interrelated. And the Powerwall is the first battery on the market to provide a solution to solar energy storage that is simple to use, easy to install, relatively inexpensive to maintain, and more aesthetically appealing than existing home batteries and storage systems, such as small diesel generators. Powerwall therefore has all the characteristics needed to succeed in this market. At least as long as the technology it is tethering itself to – solar – succeeds as well.

The advantage of Powerwall will be greater for households and business customers who have already installed solar panels and perhaps own a Tesla electric vehicle. It would allow energy produced during the day to be stored for use in the evening and early morning (including for vehicle charging). This technical interdependence with solar is something that Elon Musk, the CEO of Tesla and chairperson of SolarCity, is trying to exploit by working in close collaboration with his cousin Lyndon Rive, CEO of SolarCity, the largest rooftop solar installer the US. In this way, Tesla’s batteries could become associated with an established technology (solar power) so that the two technologies start spreading together, ultimately becoming a new technical standard adopted by the majority of households and businesses.

To support this strategy and to encourage adoption, both companies have planned not only to work together but to scale up their activities in order to control costs and make solar more affordable to their customers: Tesla has announced the opening of a $5b Nevada plant, jointly with Panasonic, and SolarCity has announced the same strategy for the large scale production of solar panels in Buffalo, New York state. SolarCity’s effort, alongside the heavily subsidized production of rooftop solar from China, will help to make the energy source more affordable, meaning there will be more demand for storage solutions like the Powerwall.

Despite the potential benefits generated by the complementarities and the technological interdependency with solar power, Tesla’s Powerwall strategy includes risks. The company may become critically dependent on the successful development of solar power, but is solar worth the bet?

In recent years, solar has been part of an increasing trend together with other renewable sources such as wind, hydro, and nuclear. However, whether solar has won the battle against alternative clean energy technologies and against fossil fuel is still highly debatable. Despite the rapid price reduction of solar panels, newly available, increasingly affordable shale gas has reduced dependence on crude oil, leading to a significant drop in both demand and price of other fossil fuels such as coal. This might slow down the uptake of alternative energy sources. In short, the shale gas revolution has introduced significant uncertainty into the future energy scenario and the adoption of solar technology is not immune from it.

Of course, the success of solar is not the only factor that will determine the Powerwall’s success. Powerwall batteries are also subject to the uncertainty about their performance in comparison with other battery technologies, and it is also possible that technological advances that could make its components obsolete.

Tesla will also have to contend with government incentives designed to spur the adoption of solar power. Net metering policies in most US states let homeowners sell excess electricity back to the utilities. In the states that adopt such regulation, the advantage of using Powerwall for storage purposes will depend on the difference between the profit consumers can make by selling energy to the grid at subsidized prices during day time and the savings that come from avoiding having to buy from the grid at night time. If energy can be sold back to the grid at a high price, it will be more attractive than energy storage for homeowners with rooftop solar. That is the reason why the 7KWh battery (priced at $3000 by Tesla) is not going to be offered by SolarCity.

Still, there are clear advantages for Tesla in entering the market for batteries for domestic and commercial energy storage. It allows Tesla to further capitalize on its knowledge and competences developed in automotive batteries for electric vehicles.

The battle for the domestic storage market has only just started and Tesla has selected a powerful ally in the solar photovoltaic (PV) sector, but both technologies are vulnerable to threats from within and outside their industry, and the reliance on solar’s success might prove a risky bet for Powerwall’s future dominance of the market for storage systems.

Should solar not become the future, Tesla’s Powerwall line won’t necessarily be doomed. 
The company might just have to pay a conversion price to fit within new standards. 

However, should it be successful, Elon Musk would not only benefit from the sales of Powerwall (and indirectly from the sales of PV produced in Buffalo by the company he is chairman of) but also from increased sales of Tesla’s own electric vehicles, the company’s core product. The latter would benefit from an easy to use recharging facility, zero emissions, and possibly a cheaper alternative to the pump. As to the question whether solar is worth the bet, overall the answer for Musk seems to be at least in the short run that it is.

Why the modern world is bad for your brain 07-07

Why the modern world is bad for your brain

In an era of email, text messages, Facebook and Twitter, we’re all required to do several things at once. But this constant multitasking is taking its toll. Here neuroscientist Daniel J Levitin explains how our addiction to technology is making us less efficient




 Daniel J Levitan: ‘When trying to concentrate on a task, an unread email in your inbox can reduce your effective IQ by 10 points.’


Our brains are busier than ever before. We’re assaulted with facts, pseudo facts, jibber-jabber, and rumour, all posing as information. Trying to figure out what you need to know and what you can ignore is exhausting. At the same time, we are all doing more. Thirty years ago, travel agents made our airline and rail reservations, salespeople helped us find what we were looking for in shops, and professional typists or secretaries helped busy people with their correspondence. Now we do most of those things ourselves. We are doing the jobs of 10 different people while still trying to keep up with our lives, our children and parents, our friends, our careers, our hobbies, and our favourite TV shows.

Our smartphones have become Swiss army knife–like appliances that include a dictionary, calculator, web browser, email, Game Boy, appointment calendar, voice recorder, guitar tuner, weather forecaster, GPS, texter, tweeter, Facebook updater, and flashlight. They’re more powerful and do more things than the most advanced computer at IBM corporate headquarters 30 years ago. And we use them all the time, part of a 21st-century mania for cramming everything we do into every single spare moment of downtime. We text while we’re walking across the street, catch up on email while standing in a queue – and while having lunch with friends, we surreptitiously check to see what our other friends are doing. At the kitchen counter, cosy and secure in our domicile, we write our shopping lists on smartphones while we are listening to that wonderfully informative podcast on urban beekeeping.

But there’s a fly in the ointment. Although we think we’re doing several things at once, multitasking, this is a powerful and diabolical illusion. Earl Miller, a neuroscientist at MIT and one of the world experts on divided attention, says that our brains are “not wired to multitask well… When people think they’re multitasking, they’re actually just switching from one task to another very rapidly. And every time they do, there’s a cognitive cost in doing so.” So we’re not actually keeping a lot of balls in the air like an expert juggler; we’re more like a bad amateur plate spinner, frantically switching from one task to another, ignoring the one that is not right in front of us but worried it will come crashing down any minute. Even though we think we’re getting a lot done, ironically, multitasking makes us demonstrably less efficient.

Multitasking has been found to increase the production of the stress hormone cortisol as well as the fight-or-flight hormone adrenaline, which can overstimulate your brain and cause mental fog or scrambled thinking. Multitasking creates a dopamine-addiction feedback loop, effectively rewarding the brain for losing focus and for constantly searching for external stimulation. To make matters worse, the prefrontal cortex has a novelty bias, meaning that its attention can be easily hijacked by something new – the proverbial shiny objects we use to entice infants, puppies, and kittens. The irony here for those of us who are trying to focus amid competing activities is clear: the very brain region we need to rely on for staying on task is easily distracted. We answer the phone, look up something on the internet, check our email, send an SMS, and each of these things tweaks the novelty- seeking, reward-seeking centres of the brain, causing a burst of endogenous opioids (no wonder it feels so good!), all to the detriment of our staying on task. It is the ultimate empty-caloried brain candy. Instead of reaping the big rewards that come from sustained, focused effort, we instead reap empty rewards from completing a thousand little sugar-coated tasks.

In the old days, if the phone rang and we were busy, we either didn’t answer or we turned the ringer off. When all phones were wired to a wall, there was no expectation of being able to reach us at all times – one might have gone out for a walk or been between places – and so if someone couldn’t reach you (or you didn’t feel like being reached), it was considered normal. Now more people have mobile phones than have toilets. This has created an implicit expectation that you should be able to reach someone when it is convenient for you, regardless of whether it is convenient for them. This expectation is so ingrained that people in meetings routinely answer their mobile phones to say, “I’m sorry, I can’t talk now, I’m in a meeting.” Just a decade or two ago, those same people would have let a landline on their desk go unanswered during a meeting, so different were the expectations for reachability.

Just having the opportunity to multitask is detrimental to cognitive performance. Glenn Wilson, former visiting professor of psychology at Gresham College, London, calls it info-mania. His research found that being in a situation where you are trying to concentrate on a task, and an email is sitting unread in your inbox, can reduce your effective IQ by 10 points. And although people ascribe many benefits to marijuana, including enhanced creativity and reduced pain and stress, it is well documented that its chief ingredient, cannabinol, activates dedicated cannabinol receptors in the brain and interferes profoundly with memory and with our ability to concentrate on several things at once. Wilson showed that the cognitive losses from multitasking are even greater than the cognitive losses from pot‑smoking.

Russ Poldrack, a neuroscientist at Stanford, found that learning information while multitasking causes the new information to go to the wrong part of the brain. If students study and watch TV at the same time, for example, the information from their schoolwork goes into the striatum, a region specialised for storing new procedures and skills, not facts and ideas. Without the distraction of TV, the information goes into the hippocampus, where it is organised and categorised in a variety of ways, making it easier to retrieve. MIT’s Earl Miller adds, “People can’t do [multitasking] very well, and when they say they can, they’re deluding themselves.” And it turns out the brain is very good at this deluding business.













































Image credit : Shyam's Imagination Libraary



 ‘Asking the brain to shift attention from one activity to another causes the prefrontal cortex and striatum to burn up oxygenated glucose, the same fuel they need to stay on task.’ Photograph: Alamy

Then there are the metabolic costs that I wrote about earlier. Asking the brain to shift attention from one activity to another causes the prefrontal cortex and striatum to burn up oxygenated glucose, the same fuel they need to stay on task. And the kind of rapid, continual shifting we do with multitasking causes the brain to burn through fuel so quickly that we feel exhausted and disoriented after even a short time. We’ve literally depleted the nutrients in our brain. This leads to compromises in both cognitive and physical performance. Among other things, repeated task switching leads to anxiety, which raises levels of the stress hormone cortisol in the brain, which in turn can lead to aggressive and impulsive behaviour. By contrast, staying on task is controlled by the anterior cingulate and the striatum, and once we engage the central executive mode, staying in that state uses less energy than multitasking and actually reduces the brain’s need for glucose.

To make matters worse, lots of multitasking requires decision-making: Do I answer this text message or ignore it? How do I respond to this? How do I file this email? Do I continue what I’m working on now or take a break? It turns out that decision-making is also very hard on your neural resources and that little decisions appear to take up as much energy as big ones. One of the first things we lose is impulse control. This rapidly spirals into a depleted state in which, after making lots of insignificant decisions, we can end up making truly bad decisions about something important. Why would anyone want to add to their daily weight of information processing by trying to multitask?

In discussing information overload with Fortune 500 leaders, top scientists, writers, students, and small business owners, email comes up again and again as a problem. It’s not a philosophical objection to email itself, it’s the mind-numbing number of emails that come in. When the 10-year-old son of my neuroscience colleague Jeff Mogil (head of the Pain Genetics lab at McGill University) was asked what his father does for a living, he responded, “He answers emails.” Jeff admitted after some thought that it’s not so far from the truth. Workers in government, the arts, and industry report that the sheer volume of email they receive is overwhelming, taking a huge bite out of their day. We feel obliged to answer our emails, but it seems impossible to do so and get anything else done.

Before email, if you wanted to write to someone, you had to invest some effort in it. You’d sit down with pen and paper, or at a typewriter, and carefully compose a message. There wasn’t anything about the medium that lent itself to dashing off quick notes without giving them much thought, partly because of the ritual involved, and the time it took to write a note, find and address an envelope, add postage, and take the letter to a mailbox. Because the very act of writing a note or letter to someone took this many steps, and was spread out over time, we didn’t go to the trouble unless we had something important to say. Because of email’s immediacy, most of us give little thought to typing up any little thing that pops in our heads and hitting the send button. And email doesn’t cost anything.

Sure, there’s the money you paid for your computer and your internet connection, but there is no incremental cost to sending one more email. Compare this with paper letters. Each one incurred the price of the envelope and the postage stamp, and although this doesn’t represent a lot of money, these were in limited supply – if you ran out of them, you’d have to make a special trip to the stationery store and the post office to buy more, so you didn’t use them frivolously. The sheer ease of sending emails has led to a change in manners, a tendency to be less polite about what we ask of others. Many professionals tell a similar story. One said, “A large proportion of emails I receive are from people I barely know asking me to do something for them that is outside what would normally be considered the scope of my work or my relationship with them. Email somehow apparently makes it OK to ask for things they would never ask by phone, in person, or in snail mail.”

There are also important differences between snail mail and email on the receiving end. In the old days, the only mail we got came once a day, which effectively created a cordoned-off section of your day to collect it from the mailbox and sort it. Most importantly, because it took a few days to arrive, there was no expectation that you would act on it immediately. If you were engaged in another activity, you’d simply let the mail sit in the box outside or on your desk until you were ready to deal with it. Now email arrives continuously, and most emails demand some sort of action: Click on this link to see a video of a baby panda, or answer this query from a co-worker, or make plans for lunch with a friend, or delete this email as spam. All this activity gives us a sense that we’re getting things done – and in some cases we are. But we are sacrificing efficiency and deep concentration when we interrupt our priority activities with email.

Until recently, each of the many different modes of communication we used signalled its relevance, importance, and intent. If a loved one communicated with you via a poem or a song, even before the message was apparent, you had a reason to assume something about the nature of the content and its emotional value. If that same loved one communicated instead via a summons, delivered by an officer of the court, you would have expected a different message before even reading the document. Similarly, phone calls were typically used to transact different business from that of telegrams or business letters. The medium was a clue to the message. All of that has changed with email, and this is one of its overlooked disadvantages – because it is used for everything. In the old days, you might sort all of your postal mail into two piles, roughly corresponding to personal letters and bills. If you were a corporate manager with a busy schedule, you might similarly sort your telephone messages for callbacks. But emails are used for all of life’s messages. We compulsively check our email in part because we don’t know whether the next message will be for leisure/amusement, an overdue bill, a “to do”, a query… something you can do now, later, something life-changing, something irrelevant.

This uncertainty wreaks havoc with our rapid perceptual categorisation system, causes stress, and leads to decision overload. Every email requires a decision! Do I respond to it? If so, now or later? How important is it? What will be the social, economic, or job-related consequences if I don’t answer, or if I don’t answer right now?




 ‘Because it is limited in characters, texting discourages thoughtful discussion or any level of detail, and its addictive problems are compounded by its hyper-immediacy.’ 

Now of course email is approaching obsolescence as a communicative medium. Most people under the age of 30 think of email as an outdated mode of communication used only by “old people”. In its place they text, and some still post to Facebook. They attach documents, photos, videos, and links to their text messages and Facebook posts the way people over 30 do with email. Many people under 20 now see Facebook as a medium for the older generation.

For them, texting has become the primary mode of communication. It offers privacy that you don’t get with phone calls, and immediacy you don’t get with email. Crisis hotlines have begun accepting calls from at-risk youth via texting and it allows them two big advantages: they can deal with more than one person at a time, and they can pass the conversation on to an expert, if needed, without interrupting the conversation.

But texting suffers from most of the problems of email and then some. Because it is limited in characters, it discourages thoughtful discussion or any level of detail. And the addictive problems are compounded by texting’s hyperimmediacy. Emails take some time to work their way through the internet and they require that you take the step of explicitly opening them. Text messages magically appear on the screen of your phone and demand immediate attention from you. Add to that the social expectation that an unanswered text feels insulting to the sender, and you’ve got a recipe for addiction: you receive a text, and that activates your novelty centres. You respond and feel rewarded for having completed a task (even though that task was entirely unknown to you 15 seconds earlier). Each of those delivers a shot of dopamine as your limbic system cries out “More! More! Give me more!”

In a famous experiment, my McGill colleagues Peter Milner and James Olds, both neuroscientists, placed a small electrode in the brains of rats, in a small structure of the limbic system called the nucleus accumbens. This structure regulates dopamine production and is the region that “lights up” when gamblers win a bet, drug addicts take cocaine, or people have orgasms – Olds and Milner called it the pleasure centre. A lever in the cage allowed the rats to send a small electrical signal directly to their nucleus accumbens. Do you think they liked it? Boy how they did! They liked it so much that they did nothing else. They forgot all about eating and sleeping. 

Long after they were hungry, they ignored tasty food if they had a chance to press that little chrome bar; they even ignored the opportunity for sex. The rats just pressed the lever over and over again, until they died of starvation and exhaustion. Does that remind you of anything? A 30-year-old man died in Guangzhou (China) after playing video games continuously for three days. Another man died in Daegu (Korea) after playing video games almost continuously for 50 hours, stopped only by his going into cardiac arrest.

Each time we dispatch an email in one way or another, we feel a sense of accomplishment, and our brain gets a dollop of reward hormones telling us we accomplished something. Each time we check a Twitter feed or Facebook update, we encounter something novel and feel more connected socially (in a kind of weird, impersonal cyber way) and get another dollop of reward hormones. But remember, it is the dumb, novelty-seeking portion of the brain driving the limbic system that induces this feeling of pleasure, not the planning, scheduling, higher-level thought centres in the prefrontal cortex. Make no mistake: email-, Facebook- and Twitter-checking constitute a neural addiction.

Analysis of coronary atherosclerosis 07-07

A histopathological analysis of the epidemiology of coronary atherosclerosis: an autopsy study


Abstract

Background

Atherosclerosis accounts for a large proportion of cardiovascular system associated morbidity and mortality. We studied the possible association between the histopathological changes of the coronary atherosclerotic lesions and the risk of sudden cardiac death (SCD) using autopsy cases.

Methods

We performed an autopsy analysis (n = 13, 4 women, 9 men mean age 67.5 years; age range 56–93 years) of SCD which occurred in patients aged over 50 years during March 2010 to December 2013. The following variables were considered: sex, age, medical history, autopsy findings to macroscopic and histological evaluation of the heart. The autopsies were performed according to standard techniques. In all subjects, the heart was dissected following standard autopsy protocol and a 5 cm section of the right coronary artery (RCA) in the atrio-ventricular groove from its origin, a 5 cm segment of the left anterior descending artery (LADA) distal to the origin of the circumflex artery, but including the region of origin of the circumflex branch and left coronary artery (LCA) from its origin till the circumflex branch were excised, dissected out, fixed in 10 % formalin, marked for identification and sent for histopathological analysis.

Results


Atherosclerotic plaques were identified in 6.5 % of specimens, 69.34 % of males and 30.66 % of female. Such plaques were typically concentric and more represented with necrosis, calcification, cholesterol crystals, and giant cells, as well as had a higher inflammatory cell count. Furthermore, intima and media thickness of coronary arteries were significantly higher in studied specimens with visualize the connective tissue layers of the adventitia and the fatty acid containing adipose cells in the periadventitial tissue. Furthermore, the degree of microscopic lesion of atherosclerosis increased proportionally with the increase in the intensity of lipid deposition and with the percentage of collagen in the atherosclerotic plaques.

Conclusion


In this study, age estimate to be a risk factor for coronary atherosclerosis in individuals more than 50 years old and may be used to predict SCD. Altogether, an enhanced understanding of the pathobiologic processes responsible for atherosclerotic changes might allow for early identification of a high-risk coronary plaque and thereby provide a rationale for innovative diagnostic and/or therapeutic strategies for the management of coronary patients and prevention of acute coronary syndromes.

Background

Coronary artery disease (CAD) is a leading cause of death of women and men worldwide. An estimated 17.5 million people died from this cause in 2005, representing 30 % of all deaths in the world; of these, 7.6 million were caused by coronary heart disease . Aging is associated with structural and functional changes of the vessel wall, which result in decreased vascular distensibility and elevated arterial stiffness . As a consequence of arterial stiffness, systolic blood pressure increases, causing a rise in left ventricular workload and subsequent hypertrophy, and diastolic blood pressure decreases, leading to an impaired coronary perfusion . Chronic systemic inflammation has been implicated in atherogenesis, and may play a role in destabilizing vulnerable coronary plaques, thereby precipitating acute thrombosis and clinical coronary vessel events.
Atherosclerosis is a pathologically diverse disease with heterogeneous mechanisms of progression. Irreversible atherosclerotic plaques begin with smooth muscle cell-rich lipid pool lesions referred to as pathologic intimal thickening and it is a lipid-driven, chronic inflammatory disease of the vessel wall in which both innate and adaptive immune responses play a role. Moreover, atherosclerosis is a complex process involving inflammation and cellular proliferation in the arterial wall that is mediated by a variety of growth factors, cytokines, thrombotic factors, and vasoactive molecules . Mature lesions exhibit calcification, which is mediated by cells similar to osteoblasts. Infectious agents may be involved in the initiation and/or progression of atherosclerotic lesions.  Roles have been suggested for a host of other factors in the etiology of atherosclerosis and of clinical events , including hemostatic factors, factors related to lipoprotein metabolism, insulin resistance , homocysteine , immune factors inflammation markers , specific fatty acids , indicators of oxidative stress, and circulating markers of endothelial function such as cellular adhesion molecules and thrombomodulin
Coronary calcium is a specific marker of atherosclerosis  that has been included in the Coronary Artery Risk Development in Young Adults Study and in subgroups in the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study . Coronary artery calcification (CAC) is a linear estimate of the total burden of coronary atherosclerosis that highly correlates with autopsy and intravascular ultrasound assessment. In fact, CAC provides a better estimate of burden of disease than luminal stenosis as determined by angiography , since less-obstructive plaques actually give rise to more occlusions than more-obstructive plaques because of their greater number. In fact, 70 % of patients with acute MI have stenosis of less than 50 % in their culprit artery on angiography. 
Therefore, stress testing (treadmill, nuclear medicine, or echo), which typically diagnoses the physiological effects of high-grade stenosis, will fail to identify a significant number of persons at risk for a hard event . CAC detection by computed tomography directly detects only hard or calcified plaque, but the calcification found essentially serves as a surrogate marker for soft or non-calcified plaque as well, since in the vast majority of patients both types of plaques coexist proportionally It should be noted that no current imaging test is able to identify plaque that is prone to rupture, and that the presence of calcification in a coronary artery does not necessarily indicate a stenosis at that site; the value of CAC assessment is, rather, in its ability to reflect the overall burden of coronary atherosclerosis.
The objective of the study was to determine the possible association between the histopathological changes of the coronary atherosclerotic lesions and the risk of sudden cardiac death (SCD) and acute myocardial infarction (AMI) using autopsy cases.

Methods

This study was conducted from March 2010 to December 2013 in the General Mortuary based at the Tehran forensic medicine center with various causes of death (sudden cardiac death and myocardial infarction).

Study objects and specimen preparation


This study was approved by the local ethics committee. The hearts of 13 patients (4 women, 9 men mean age 67.5 years; age range 56–93 years) were collected at autopsy within 8 h after death. Inclusion criteria were age over 50 years and an autopsy had to be intended. All cause of death were sudden cardiac death and acute myocardial infarction (n = 13). A signed letter of consent was taken from the relatives of the dead bodies. Human hearts were obtained from a pathologic study of sudden cardiac death due to atherosclerosis and coronary artery thrombosis. After explanation from the corpse, the hearts were washed in water without further fixation or staining.

Preparation of the coronary arteries


The heart was dissected following standard autopsy protocol at autopsy. The coronary arteries were cannulated, washed with 0.1 mol/L PBS (pH 7.4), and perfused with 1 L of freshly prepared 4 % (wt/vol) paraformaldehyde in 0.1 mol/L sodium phosphate (pH 7.4) at 100 mmHg. Next, the heart was immersed in 4 % paraformaldehyde for at least 24 h at 4°C. A 5 cm section of the right coronary artery (RCA) in the atrio-ventricular groove from its origin, a 5 cm segment of the left anterior descending artery (LADA) distal to the origin of the circumflex artery, but including the region of origin of the circumflex branch and left coronary artery (LCA) from its origin till the circumflex branch were excised and dissected out. All the sections of coronary arteries from each case were fixed in 10 % formalin, marked for identification and sent for histopathological analysis. Paraffin sections were made and the sections stained using Hematoxylin and Eosin (H & E) dyes.

Histopathological examination


In all subjects, the heart was fixed with 10 % formalin. All specimens of coronary arteries were taken from each heart for histopathological examination. Twenty-six blocks from the right and left coronary artery were cut into 5-μm-thick serial sections and each section was stained with hematoxylin and eosin stains. When necessary, samples were partially decalcified by acid extraction before sectioning. The atherosclerotic lesion type of each section was carefully classified by 2 investigators simultaneously using a double-headed light microscope.

Grading atherosclerosis by pathologists


Two pathologists independently estimated the percentage of the tunica intimal and medial surfaces area involved with fatty streaks and raised lesions in the coronary arteries. The consensus lesion grade was the average of the grades of 2 pathologists and raised lesions mostly included an area of hemorrhage, thrombosis, ulceration, or calcification.

Results

Histopathologically, moderate to severe atheromatous lesions were observed in the coronary arteries. The subendothelial space was dilated by an extracellular network containing large amounts of fibrin/collagen composite materials in sections stained with H&E.
In some cases, a numerous number of macrophages and occasionally lymphoplasmacyte-rich infiltrates were detected in the subendothelial space with lipid deposition. The intimal and medial smooth muscle cells usually had swollen nuclei and abundant cytoplasm. In most cases, severe atheromatous lesions containing abundant chronic inflammatory cells infiltration (Lymphocytes were the dominant inflammatory cells) and calcium deposits were frequently observed in the tunica media and adventitia of coronary arteries . These histologic changes were consistent with atherosclerotic deposits, early aneurysm formation, and chronic and acute hemorrhage.
thumbnailFig. 1. Micrographs showing the coronary tree from patients who died of acute myocardial infarction (AMI) . Panel (a) demonstrates the fatty deposits in adventitia and inflammatory cells surrounding the media of this arteriole are seen (H&E, 200 Ҳ). Panel (b) shows the deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media together with severe narrowing by atherosclerotic plaque, with several hemorrhagic necrotic cores (H&E, 400 Ҳ). Panel (c) indicates histologic finding with fibrous tissue, and necrotic core (H&E, 400 Ҳ). Panel (d) shows microscopic section of the coronary artery shows thickening of the vascular wall by atherosclerotic deposits and hemorrhage. (H&E, 200 Ҳ)
thumbnailFig. 2. Micrographs showing the three major epicardial coronary arteries from patients from the who died of a sudden cardiac ischemic death. Panel (a) demonstrates severe atheromatous lesions, calcium deposits of luminal atherosclerotic plaques with hemorrhage, hyaline material in the tunica media (H&E, 200 Ҳ). Panel (b); Photomicrograph of a coronary plaque (H&E stain) showing intraplaque hemorrhage with the necrotic core with a form of calcification that result in irregular nodules of calcium (H&E, 200 Ҳ). Panel (c) indicates a prevalently fibrous plaque characterized by a necrotic core associated with a thick fibrous and this photograph of coronary plaques demonstrates multiple necrotic cores (H&E, 400 Ҳ). Panel (d) shows occasionally lymphoplasmacyte-rich infiltrates and fibroproliferative tissue together with areas of free cholesterol crystals (H&E, 400 Ҳ)
thumbnailFig. 3. Histopathological localization of atherosclerotic lesions of the human coronary artery. Panel (a) shows the bright luminal fibrous layers in the atherosclerotic plaque with the resolution obtained together with the minimal obstruction to the coronary lumen caused by atherosclerotic plaque (H&E, 200 Ҳ). . Panel (b) Magnification × 200, H&E stain. An un-normal coronary wall. Note thickened media, which contained cholesterol crystals within the tunica media together with lesions with fibromuscular fibrous. Panel (c): Photomicrograph of thick part of atheroma and shows extracellular lipid forms a confluent core in the musculoelastic layer of eccentric adaptive thickening that is always present in this location and the lipid core also contains cholesterol crystals and dark staining aggregates of microcrystalline calcium (H&E, 400 Ҳ). Panel (d) demonstrates severe atheromatous lesions containing abundant lymphocytes cells infiltration and the deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media (H&E, 400 Ҳ)
Numerous macrophages with foamy cytoplasm infiltrated the tunica intima and media . In severe lesions, the tunica media contained enlarged macrophages with foamy cytoplasm, hyaline material, fibrofatty plaque. and mineralized material  The lesions were characterized by the deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media, sometimes forming fibrofatty plaques , containing abundant cholesterol clefts  and mineralized material. The lesions started in the tunica intima and extended to the tunica media and tunica adventitia. In some cases, lesions were characterized by dense intimal fibrosis with necrotic debris and foam cells typical of atherosclerosis. Restenotic lesions were characterized by an increased proportion of loose fibroproliferative tissue, as well as all types of lesion pathology were observed in proximal, mid, distal and branch segments in these 13 cases. However, proximal lesions were more commonly atheromatous plaques  as compared with distal narrowing’s.
Moreover, the combination of densely layered collagen and degenerating tissue was significantly more common in specimens from pathologic lesions, whereas loosely arranged proliferative tissue was significantly more common in tissue from atherosclerotic lesions . Furthermore, the study has revealed that ruptured plaques of human autopsied affected were characterized by the presence of a more severe inflammatory infiltrate, constituted by monocytes, macrophages, and lymphocyte cells. Areas of necrosis and the existence of giant cells were also more frequent in segments with luminal atherosclerotic plaques. Inflammatory cells were more abundant within segments with luminal atherosclerotic plaques Calcium deposits were more commonly seen in segments containing luminal atherosclerotic plaques . 
Whereas the presence of calcium deposits had an excellent specificity of luminal atherosclerotic plaques, the majority of atherosclerotic plaques were not calcified, and hence, sensitivity was much lower. Although we had not stained the internal elastic lamina because of extreme superficiality of the calcified areas, we supposed that most of them were intimal in location. In the present study, calcium in the coronary plaque is often fragmented and may be located deep in the plaque or close to the surface. However the frequency of calcified nodules (with surface thrombus), a form of calcification that results in irregular nodules of calcium , is higher in coronary disease.
Finally, the most important findings were the presence of pseudocalcium–calcium (pCa–Ca) deposits and arterial wall degeneration. Proliferative lesions have been found in the coronary arteries of thirteen specimens of human autopsy. In the present study, 69.34 % of male showed atherosclerosis and 30.66 % of female showed atherosclerosis.

Discussion

Atherosclerosis is a disease of large- and medium-sized muscular arteries, characterized by inflammation of smooth muscle cells and formation of atherosclerotic plaques composed of necrotic cores; calcium deposits; and an accumulation of modified lipids, endothelial cells, leukocytes, and foam cells . Many components of the vascular, metabolic, and immune systems are involved in this process . Buildup of material and infiltrates leads to vascular remodeling, acute and chronic luminal obstruction, abnormalities of blood flow, and diminished oxygen supply to target organs. In human beings, atherosclerosis is the most common pathologic process leading to cardiovascular disease
The autopsy study provides a means of understanding the basic process which sets a stage for clinically significant atherosclerotic cardiovascular disease. There is no valid method of sampling of living population. It was, therefore, considered that death suspected due to cardiovascular pathology, probably provide the best sample of the living population for studying atherosclerosis.
In this study, the histological examination of the serially sectioned coronary arteries from 13 men and women who died suddenly and unexpectedly revealed the frequent presence of early atherosclerotic lesions in 13 cases. The lesions are marked by infiltration in the intima and media of coronary artery, monocytes/foam cells, rich-lymphocytes and deposits of mineral material, mainly composed of cellular matrix network, as well as fragmentation of the elastic fiber system.
Age is a powerful risk factor for coronary heart disease. The development of atherosclerosis increases markedly with age up to an age of about 65, regardless of sex and ethnic background. The autopsy findings of coronary arthrosclerosis in different reports are variable in relation of age and sex. In an autopsy study by Thomas et al. among 124 men (age range, 50 to 69 years) who died of non - cardiac causes, 10.3 % had one-vessel, 2.8 % had two-vessel, and 1.4 % had three-gmale in age group between 52 and 83 years. This prevalence of coronary atherosclerosis is higher but supported by other investigators. The coronary atherosclerosis is also increasing with rapid pace in older age group also.
Autopsies performed on casualties of the Korean War revealed coronary artery involvement in 77.3 % of the hearts studied, and data after the Vietnam War noted the presence of atherosclerosis in 45 % of casualties with severe disease in 5 %. One hundred eleven victims of non-cardiac trauma underwent pathologic examination of their coronary arteries to estimate the presence and severity of coronary atherosclerosis. Sudden coronary death (SCD) in older individuals is generally associated with extensive coronary atherosclerosis, although it may be the first manifestation of ischemic heart disease. In younger age-groups, SCD may occur in the presence of less severe disease 
Low-density lipoprotein remains the most important risk factor for development of atherosclerosis in humans and has been also associated with atherosclerosis in animals ]. However, immune and inflammatory mechanisms of atherosclerosis have gained tremendous interest in the past 20 years . New data suggest an important role for chemokine’s and chemokine receptors in atherosclerosis and highlight a network of cytokines that modulate the immune response and inflammation of the arterial wall . Because it has been shown in humans that all phases of atherosclerosis are regulated by inflammatory mechanisms, the possible impact of chronic inflammation in the development of atherosclerosis in animals and the importance of preventive diagnosis should be considered 
In our study, an increased number of inflammatory cells, the presence of giant cells and areas of necrosis and calcification were more frequent in segments containing atherosclerotic plaques, consistent with findings from studies on atherosclerosis of coronary arteries]. Moreover, lymphocytes were more abundant in sections containing atherosclerotic plaques. However, contrary to what has been reported from the analysis of arterial plaques , in our study, lymphocytes were the predominant inflammatory cells in the majority of atherosclerotic plaques. 
The findings of a study by van der Wal et al. also suggested a predominance of lymphocytes in venous compared with arterial plaques. Although the reasons for a predominance of lymphocytes in vessel atherosclerotic lesions need further investigation, it has been suggested that dendritic cells and lymphocytes co-accumulate in atherosclerotic vein grafts, suggesting an immune-mediated antigen presentation to lymphocytes It might be the case that in human venous plaques, lymphocytes are dominant inflammatory cells that render the venous plaques more vulnerable to rupture or disruption because of interferon- production, which reduces the fibrous cap thickness 
In the present study, it was observed that nine cases (69.34 %) were males and 4 (30.66 %) were females, which are concordant with other researchers findings that showed 74.8 % males and 24.2 % females, and another study found 66.5 % males and 33.5 % females . In the present study, 69.34 % of male showed atherosclerosis & 30.66 % of female showed atherosclerosis which are concordant with the study of Thej et al., showed 62 % were males & 50 % were females in Indian population  Study reported by Yazdi SAT et al., showed 73 % males and 61 % females had atherosclerosis in a population of Iran. This difference is again explained by the demographic, geographic, racial, lifestyle & dietary variation in population Singh H et al., have reported the incidence of atherosclerosis in the coronaries to be 68 % in males and 27 % in females 
Coronary artery calcium (CAC) has been demonstrated to be associated with the risk of coronary heart disease. Our study showed that the information provided here can be used to examine whether a patient has a high CAC score relative to others with the same age, gender, and race/ethnicity who do not have clinical cardiovascular disease or treated diabetes. Rumberger et al. have made additional recommendations for specific cut points for mild, moderate, and severe coronary artery calcium that have been used frequently in clinical practice. The ACC/ In contrast, a “high” calcium score indicates greater likelihood of disease and may be consistent with moderate to high risk of a cardiovascular event during that time period. However, some post-mortem pathologic analyses of coronary arteries reported that calcium was a frequent feature of plaque rupture. Other reports have been shown that ruptured plaques were less likely to be calcified in acute coronary syndrome patients . Thus, coronary calcium is not a marker for neither unstable nor stable plaques.
If calcium does have a different impact on risk depending on race, then the observed CAC should be evaluated relative to subjects of the same age, gender, and race/ethnicity, as presented here. It is premature to use percentiles from either this study or others to make medical decisions. In other words, at this time, the information presented here cannot necessarily be used to conclude that a patient is “high risk” but can indicate whether they have a high calcium score relative to others with the same age, gender, and race/ethnicity.
Atherosclerosis and coronary artery disease are huge health concerns in Iran. They constitute the largest single cause of death and exact a financial burden of billions of dollars annually. It is well known that lifestyle modification and drug therapy in selected individuals can reduce the risk of hard cardiac events, but current Framingham risk assessment is suboptimal.

Conclusions

Our study suggested that although calcification is found more frequently in advanced lesions, it may also occur in small amounts in earlier lesions, which appear in the second and third decades of life. Histopathological investigation has shown that plaques with microscopic evidence of mineralization are larger and associated with larger coronary arteries than plaques or arteries without calcification. The relation of arterial calcification to the probability of plaque rupture is unknown. Although the amount of coronary calcium correlates with the amount of atherosclerosis in different individuals and to a lesser extent in segments of the coronary tree in the same individuals, it is not known if the quantity of calcification tracks the quantity of atherosclerosis over time in the same individuals. Further research is needed to better elucidate the relation of calcification to the pathogenesis of both atherosclerosis and plaque rupture.
Finally, histopathological studies provide the most accurateclues to a better understanding of human coronary artery disease. With better insight into disease pathophysiology, novel interventions could be introduced to improve care and future outcomes for patients undergoing coronary artery disease.

Abbreviations

CAD: Coronary artery disease
CAC: Coronary artery calcium
SCD: Sudden coronary death
AMI: Acute myocardial infarction