Evaluation of Data Entry Errors and Data Changes to an Electronic Data Capture Clinical Trial Database

 

 

Jules T. Mitchel, Yong Joong Kim, Joonhyuk Choi, Glen D Park, Silvana Cappi, David Horn, Morgan Kist, Ralph B. D’Agostino, Dr. Mitchel is President of Target Health Inc.

 

 

 

Source: Drug Information Journal 2011;45(4):421-430

 

Abstract

 

Monitoring of clinical trials includes several disciplines, stakeholders, and skill sets. The aim of the present study was to identify database changes and data entry errors to an electronic data capture (EDC) clinical trial database, and to assess the impact of the changes. To accomplish the aim, Target e*CRF was used as the EDC tool for a multinational, dose-finding, multicenter, double-blind, randomized, parallel, placebo-controlled trial to investigate efficacy and safety of a new treatment in men with lower urinary tract symptoms associated with benign prostatic hyperplasia. The main errors observed were simple transcription errors from the paper source documents to the EDC database. This observation was to be expected, since every transaction has an inherent error rate. What and how to monitor must be assessed within the risk-based monitoring section of the comprehensive data monitoring plan. With the advent of direct data entry, and the elimination of the requirement to transcribe from a paper source record to an EDC system, error rates should go down dramatically. In addition, protocol violations and data outside the normal range can be identified at the time of data entry and not days, weeks, and months after the fact.

 

Medscape.com, by Laurie Barclay MD, July 5, 2011 — Women who sat for long periods of time every day were 2 to 3 times more likely to develop idiopathic pulmonary embolism than more active women, according to the results of a prospective cohort study published online July 4 in the British Medical Journal.

 

 

“Associations between physical inactivity, physical activity, and pulmonary embolism remain uncertain,” write Christopher Kabrhel, MD, attending physician and assistant professor of surgery, Department of Emergency Medicine, Massachusetts General Hospital, Boston, and colleagues.

“Some published case-control studies found that exercising on a regular basis decreases the risk of venous thrombosis by 30-50% compared with not exercising. Other studies, however, including prospective cohort studies, have found that physical activity is associated with an increased risk of venous thromboembolism.”

Using the Nurses’ Health Study cohort of 69,950 female nurses who completed biennial questionnaires from 1990 to 2008, the investigators aimed to examine the association between sedentary lifestyle and incident idiopathic pulmonary embolism. The main study endpoint was idiopathic pulmonary embolism documented by medical records review.

Using multivariable Cox proportional hazards models, the investigators controlled for age, body mass index, energy intake, smoking status, pack-years, race, spouse’s educational level, parity, menopause, nonaspirin nonsteroidal anti-inflammatory drugs, warfarin, multivitamin supplements, hypertension, coronary heart disease, rheumatological disease, and dietary patterns. The main exposure evaluated was physical inactivity (hours of sitting per day), and the secondary exposure was physical activity (metabolic equivalents per day).

There were 268 episodes of incident idiopathic pulmonary embolism during the 18-year study period. Time spent sitting each day was directly associated with risk for idiopathic pulmonary embolism (in combined data, 41/104,720 for the most inactive women compared with 16/14,565 for the least inactive women; P < .001 for trend).

Compared with women who spent the least time sitting, women who spent the most time sitting had more than double the risk for pulmonary embolism (multivariable hazard ratio, 2.34; 95% confidence interval, 1.30 – 4.20). Physical activity was not associated with pulmonary embolism (P = .53 for trend).

“Physical inactivity is associated with incident pulmonary embolism in women,” the study authors write. “Interventions that decrease time sitting could lower the risk of pulmonary embolism.”

Limitations of this study include its low generalizability to nonwhite racial/ethnic groups, to men, and to younger women; use of self-reported time sitting as a proxy measure for physical inactivity; and inability to detect any changes in physical inactivity. Other limitations were failure to control completely for warfarin use, measurement bias, investigation bias, and reliance on self-report for measurement of physical inactivity.

In an accompanying editorial, James D. Douketis, MD, and Alfonso Iorio, MD, from McMaster University in Hamilton, Ontario, Canada, note that the findings, if valid, may have major public health implications.

“Overall, the study reinforces the notion that prolonged inactivity increases the risk of [venous thromboembolism], and it shows how this occurs in everyday life,” Dr. Douketis and Dr. Iorio write. “The findings also indirectly support the use of preventive interventions for at risk people with prolonged immobility, typically patients in hospital, in whom anticoagulants to prevent [venous thromboembolism] remain underused. For otherwise healthy people, the take home message may be to apply the ancient Greek proverb of ‘métron áriston’ or ‘moderation is best’ to both our activity and inactivity.”

The National Institute on Aging, National Institutes of Health, Bethesda, Maryland, supported this study. The study authors and editorialists have disclosed no relevant financial relationships.

BMJ. Published online July 4, 2011

 

Should you feel any chest pain, call 911 immediately or have someone take you to the closest hospital’s emergency department right away.

Pulmonary embolism is difficult to diagnose from a medical perspective, even with the most recent checks and equipment available. For that reason, you should not attempt to diagnose yourself or deal with yourself at dwelling and should seek rapid care and analysis in an emergency department.

Pulmonary embolism has the potential to be fatal. For those who suspect that you’ve a pulmonary embolism, you should seek fast medical attention within the emergency department.

 

 

How Is Pulmonary Embolism Diagnosed?

Pulmonary embolism (PE) is diagnosed based on your medical history, a physical exam, and test results.

Doctors who treat patients in the emergency room often are the ones to diagnose PE with the help of a radiologist. A radiologist is a doctor who deals with x rays and other similar tests.

Medical History and Physical Exam

To diagnose PE, the doctor will ask about your medical history. He or she will want to:

  • Find out your deep vein thrombosis (DVT) and PE risk factors
  • See how likely it is that you could have PE
  • Rule out other possible causes for your symptoms

Your doctor also will do a physical exam. During the exam, he or she will check your legs for signs of DVT. He or she also will check your blood pressure and your heart and lungs.

Diagnostic Tests

Many tests can help diagnose PE. Which tests you have will depend on how you feel when you get to the hospital, your risk factors, available testing options, and other conditions you could possibly have. You may have one or more of the following tests.

Ultrasound

Doctors can use ultrasound to look for blood clots in your legs. Ultrasound uses sound waves to check blood flow in your veins.

For this test, gel is put on the skin of your legs. A hand-held device called a transducer is moved back and forth over the affected areas. The transducer gives off ultrasound waves and detects their echoes as they bounce off the vein walls and blood cells.

A computer turns the echoes into a picture on a computer screen, allowing the doctor to see blood flow in your legs. If the doctor finds blood clots in the deep veins of your legs, he or she will recommend treatment.

DVT and PE both are treated with the same medicines.

Computed Tomography Scans

Doctors can use computed tomography (to-MOG-rah-fee) scans, or CT scans, to look for blood clots in the lungs and legs.

For this test, dye is injected into a vein in your arm. The dye makes the blood vessels in your lungs and legs show up on x-ray images. You’ll lie on a table, and an x-ray tube will rotate around you. The tube will take pictures from many angles.

This test allows doctors to detect most cases of PE. The test only takes a few minutes. Results are available shortly after the scan is done.

Lung Ventilation/Perfusion Scan

A lung ventilation/perfusion scan, or VQ scan, uses a radioactive substance to show how well oxygen and blood are flowing to all areas of your lungs. This test can help detect PE.

Pulmonary Angiography

Pulmonary angiography (an-jee-OG-rah-fee) is another test used to diagnose PE. This test isn’t available at all hospitals, and a trained specialist must do the test.

For this test, a flexible tube called a catheter is threaded through the groin (upper thigh) or arm to the blood vessels in the lungs. Dye is injected into the blood vessels through the catheter.

X-ray pictures are taken to show blood flowing through the blood vessels in the lungs. If a blood clot is found, your doctor may use the catheter to remove it or deliver medicine to dissolve it.

Blood Tests

Certain blood tests may help your doctor find out whether you’re likely to have PE.

A D-dimer test measures a substance in the blood that’s released when a blood clot breaks down. High levels of the substance may mean a clot is present. If your test is normal and you have few risk factors, PE isn’t likely.

Other blood tests check for inherited disorders that cause blood clots. Blood tests also can measure the amount of oxygen and carbon dioxide in your blood. A clot in a blood vessel in your lungs may lower the level of oxygen in your blood.

Other Tests

To rule out other possible causes of your symptoms, your doctor may use one or more of the following tests.

  • Echocardiography (echo). This test uses sound waves to create a moving picture of your heart. Doctors use echo to check heart function and detect blood clots inside the heart.
  • EKG (electrocardiogram). An EKG is a simple, painless test that detects and records the heart’s electrical activity.
  • Chest x ray. This test creates pictures of your lungs, heart, large arteries, ribs, and diaphragm (the muscle below your lungs).
  • Chest MRI (magnetic resonance imaging). This test uses radio waves and magnetic fields to create pictures of organs and structures inside the body. MRI often can provide more information than an x ray.

 

 

 

 

BMJ 2011; 343:d3865 doi: 10.1136/bmj.d3865 (Published 4 July 2011)

Cite this as: BMJ 2011; 343:d3865

Editorial

The association between venous thromboembolism and physical inactivity in everyday life

  1. 1. James D Douketis, MD1,
  2. 2. Alfonso Iorio, MD2

+ Author Affiliations

  1. 1. 1Vascular Medicine, McMaster University, Hamilton, ON, Canada, L8N 4A6
  2. 2. 2Health Information Research Unit, Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, ON, Canada
  3. jdouket@mcmaster.ca

Seems to be small and slightly higher than that for oral contraceptive use

Observational studies have shown that several lifestyle choices and habits, such as eating too much refined sugar or drinking more than one glass of wine a day, may have adverse health effects. 1 2 The linked prospective cohort study by Kabrhel and colleagues (doi: 10.1136/bmj.d3867 ) adds inactivity to this list of sins. 3 The study followed 69 950 female nurses for an average of 18 years. Those women who were the most inactive, defined by the number of hours of sitting a day (>41 hours a week outside of work), were two to three times more likely to develop otherwise unprovoked venous thromboembolism (VTE), which manifested as pulmonary embolism, than women who spent the least amount of time sitting (<10 hours a week outside of work). The association remained robust after controlling for other risk factors for VTE such as increasing age, body mass index, and concomitant disease, and was not mitigated by periods of physical activity and exercise.

If the findings are valid they may have major public health ramifications. The study also showed that physical inactivity correlated with coronary heart disease (spanning from 1.2% to 5.1% across fifths of physical inactivity) and hypertension (from 18% to 25%). Prolonged periods of physical inactivity could be …

 

 

 

Serena Williams Battles a Pulmonary Embolism and a Hematoma

 

 

Medical Author: Melissa Conrad Stoppler MD

Medical Editor: William C. Shiel Jr. MD, FACP, FACR

 

 

 

MedicineNet.com  —  Whenever a young and healthy athlete gets sick, it always gets the attention of the press. The news is even more dramatic when the condition can be life-threatening, as in the case of Serena Williams, who reportedly developed a pulmonary embolism in late February 2011. While it is possible to recover fully from a pulmonary embolism, it is indeed a serious condition and requires serious medications. In addition, Ms. Williams also reportedly required treatment for a hematoma, a collection of clotted blood that forms outside of a blood vessel.

A pulmonary embolism (PE) happens when a blood clot (thrombus) forms in the one of the body’s large veins (known as deep vein thrombosis or DVT), breaks off, and travels (embolizes) in the circulatory system back to the heart and out into the arteries that carry blood to the lungs to load up oxygen. There the clot in the lungs (embolus) then clogs the artery that provides blood supply to part of the lung, preventing the normal exchange of oxygen and carbon dioxide. It also reduces the blood supply to the lung tissue itself. Lung tissue can die (infarct) if circulation is impaired.

Essentially anything that increases the potential for blood clots to form in the veins can increase your chances of developing a pulmonary embolus. While some medications and chronic medical problems can increase the tendency of blood to clot, even those who are healthy and fit can be at risk for pulmonary embolism due to prolonged immobilization (as with extended car or plane travel or hospitalization and bed rest) or circumstances that damage the blood vessel walls, making a clot more likely to form. Surgery and trauma to the leg are examples of conditions that can make a vein more likely to clot. Sudden chest pain and shortness of breath are the main symptoms of pulmonary embolism, but coughing may also occur. The pain is usually worse when taking a breath (known as pleurisy). The affected individual may have signs such as a blue-tinged discoloration of the skin and feel lightheaded or weak. In severe cases, the heart stops beating and sudden death results. Fortunately, treatment for pulmonary embolism is available, and most patients survive when appropriately diagnosed and treated with anti-clotting drugs. A higher incidence of death from pulmonary embolism occurs in patients who are older, have other underlying illnesses, or have a delay in diagnosis.

Photo Credit: Brent Holland

 

 

 

The New York Times, July 6, 2011, by Gretchen Reynolds  —  Why does exercise make us happy and calm? Almost everyone agrees that it generally does, a conclusion supported by research. A survey by Norwegian researchers published this month, for instance, found that those who engaged in any exercise, even a small amount, reported improved mental health compared with Norwegians who, despite the tempting nearness of mountains and fjords, never got out and exercised. A separate study, presented last month at the annual meeting of the American College of Sports Medicine, showed that six weeks of bicycle riding or weight training eased symptoms in women who’d received a diagnosis of anxiety disorder. The weight training was especially effective at reducing feelings of irritability, perhaps (and this is my own interpretation) because the women felt capable now of pounding whomever or whatever was irritating them.

But just how, at a deep, cellular level, exercise affects anxiety and other moods has been difficult to pin down. The brain is physically inaccessible and dauntingly complex. But a recent animal study from researchers at the National Institute of Mental Health provides some intriguing new clues into how exercise intertwines with emotions, along with the soothing message that it may not require much physical activity to provide lasting emotional resilience.

For the experiment, researchers at the institute gathered two types of male mice. Some were strong and aggressive; the others were less so. The alpha mice got private cages. Male mice in the wild are territorial loners. So when then the punier mice were later slipped into the same cages as the aggressive rodents, separated only by a clear partition, the big mice acted like thugs. They employed every animal intimidation technique and, during daily, five-minute periods when the partition was removed, had to be restrained from harming the smaller mice, which, in the face of such treatment, became predictably twitchy and submissive.

After two weeks of cohabitation, many of these weaker mice were nervous wrecks. When the researchers tested them in a series of stressful situations away from the cages, the mice responded with, as the scientists call it, “anxiety-like behavior.” They froze or ran for dark corners. Everything upset them. “We don’t use words like ‘depressed’ to describe the animals’ condition,” said Michael L. Lehmann, a postdoctoral fellow at the institute and lead author of the study. But in effect, those mice had responded to the repeated stress by becoming depressed.

But that was not true for a subgroup of mice that had been allowed access to running wheels and nifty, explorable tubes in their cages for several weeks before they were housed with the aggressive mice. These mice, although wisely submissive when confronted by the bullies, rallied nicely when away from them. They didn’t freeze or cling to dark spaces in unfamiliar situations. They explored. They appeared to be, Dr. Lehmann said, “stress-resistant.”

“In people, we know that repeated applications of stress can lead to anxiety disorders and depression,” Dr. Lehmann said. “But one of the mysteries” of mental illness “is why some people respond pathologically to stress and some seem to be stress-resistant.”

To discern what was different, physiologically, about the stress-resistant mice, the scientists looked at brain cells using stains and other techniques. They determined that neurons in part of the rodents’ medial prefrontal cortex, an area of the brain involved in emotional processing in animals and people, had been firing often and rapidly in recent weeks, as had neurons in other, linked parts of the brain, including the amygdala, which is known to handle feelings of fear and anxiety.

The animals that had not run before moving in with the mean mice showed much less neuronal activity in these portions of the brain.

Dr. Lehmann said that he believed that the running was key to the exercised animals’ ability to bounce back from their unpleasant housing conditions.

Of course, as we all know, mice are not people. But the scientists believe that this particular experiment is a fair representation of human interpersonal relations, Dr. Lehmann said. Hierarchies, marked by bullying and resulting stress,  are found among people all the time. Think of your own most dysfunctional office job. (Interestingly, the same experiment cannot be conducted on female mice, who like being housed together, Dr. Lehmann said, so he and his colleagues are testing a female-centric version, in which “cage mates are swapped out continuously,” to the consternation and grief of the female mice left behind.)

Perhaps best of all, Dr. Lehmann does not believe that hours of daily exercise are needed or desirable to achieve emotional resilience. The mice in his lab ran only when and for as long as they wished, over the course of several weeks. Other animal experiments have intimated that too much exercise could contribute to anxiety, and Dr. Lehmann agrees that that outcome is possible. Moderate levels of exercise seem to provide the most stress-relieving benefits, he said. Dr. Lehmann does not have a car and walks everywhere, and although he lives in Washington, a cauldron of stress induction, he describes himself as a “pretty calm guy.”

 

 

 

 

Does Exercise Really Boost Your Mood?

By GRETCHEN REYNOLDS

Lawrence Wee/Getty

 

 

 

There exists a large and soothing body of scientific literature suggesting that regular exercise can improve someone’s mood and fight anxiety. And then there is this experiment from Germany, in which researchers placed running wheels in the cages of a group of laboratory mice and let them exercise at will.

Mice generally love to run, and these rodents spent almost every waking hour on their wheels, skittering through more miles than most animals are allowed to complete during exercise studies, averaging about seven miles per mouse per day. The scientists, from the Central Institute of Mental Health Mannheim, then placed these avid runners in unfamiliar situations. What they found was surprising, in part because it contradicted earlier experiments by other researchers. The mice froze or quickly fled to dark corners, behaviors considered by some researchers to signify anxiety. It was as if the marathon runners in this experiment had become more anxious and neurotic than the nonrunners, presumably because of the volume of their running.

The apparent implication of that finding — that too much running makes an animal a nervous wreck — might seem disconcerting. But as this study, published in the journal Hippocampus, and additional new research makes clear, a great deal still needs to be understood about just how exercise affects mood.

To date, most research into the interplay of exercise and anxiety has focused on the actions of various neurotransmitters or chemical messengers within the brain, like serotonin and dopamine. But the German researchers weren’t looking at neurotransmitters. Their interest was in a different brain mechanism. They were trying to determine whether the formation of new brain cells, a process called neurogenesis, was making their lab animals nervous.

Exercise spurs neurogenesis, a finding confirmed by seminal research completed a few years ago. This neurogenesis would seem to be completely laudable, since it occurs mostly in the hippocampus, a portion of the brain associated with memory and thinking. Rodents that have exercised and that have brains fizzing with new neurons tend to score well on tests of memory and cognition.

But the effects of neurogenesis on mood are murkier. A number of neurological case studies have reported that people and animals with lesions in the hippocampus — meaning fewer brain cells in that region — are less prone to anxiety than other people.

So could high volumes of running and the commensurately large amounts of neurogenesis in the hippocampus produce anxiety? The German work seemed to say yes, particularly a follow-up experiment by the same scientists published in September in the online journal PLoS One. In that study, the researchers radiated the brains of mice to prevent neurogenesis, and then let them run. The treated mice eagerly took to their wheels, but grew almost no new neurons. Afterward, placed in stressful situations, they remained calm, reacting much like sedentary mice.

It seemed that neurogenesis had been the culprit behind the earlier runners’ excessive anxiety.

But the scientists are quick to point out that these findings do not mean that human marathon and ultramarathon runners are necessarily at risk of developing mood problems. The “exercise schedule of mice is not comparable to human fitness training,” wrote Dr. Johannes Fuss and Dr. Peter Gass, the primary authors of the two studies, in a shared e-mail response to questions. With very rare exceptions, humans will not spend their entire waking hours running.

More important, it’s not clear whether the behavior of the nervous mice was necessarily anxiety as we might experience it. The exercised mice did frequently freeze and hide, but they are prey animals, a situation that does not reward insouciance. To be less anxious, if you are a mouse, Dr. Fuss and Dr. Gass wrote, “might not always be the best survival strategy.”

The German scientists, in focusing narrowly on neurogenesis, may also have underestimated the intricate and broad ways in which exercise affects the brain’s mood centers. A fascinating series of experiments conducted at Princeton University and presented at the 2010 annual meeting of the Society for Neuroscience in November showed that neurons born from running actually behave differently from other neurons. They are not as physiologically excitable, even in stressful situations. The Princeton scientists showed that after a rodent stress test, the hippocampi of running mice contained fewer proteins associated with neuron activity than the brains of sedentary mice, even though the runners had more neurons over all. The runners’ brain cells had remained, it seemed, more calm in the face of stress. Similarly, the scientists found, areas of the brain that would normally shoot stimulating messages to the hippocampus during and after stress were quieter in exercised mice.

“Thus,” the Princeton researchers concluded, “running may reduce anxiety-like behavior” despite increasing the number of new brain cells. Exercise had recalibrated the animals’ brains so that they were more serene.

What this emerging science means for those of us who regularly exercise is, admittedly, still being teased out by researchers. But other recent studies are encouraging. A review article published last year in The Archives of Internal Medicine, for instance, concluded that compared with sloth, “exercise training significantly reduced anxiety symptoms” in a group of people at risk for mood problems. And in a beguiling experiment also presented at the 2010 Society for Neuroscience meeting, scientists from Oklahoma State University found that female rats allowed to run at a moderate pace for 10 to 60 minutes several times a week — my exercise regimen, in fact — behaved with robust mental health in stress tests. So whether you run on two legs or four, the message may be: relax.

 

 

Medscape.com, by Michael O;Riordan, July 6, 2011 (Aarhus, Denmark) — Nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors are associated with an increased risk of atrial fibrillation or flutter, according to the results of a new population-based, case-control study [1]. The study adds evidence that these arrhythmic risks should be added to the overall CV risks when considering prescribing NSAIDs, say researchers.

“It’s important to know that the absolute risk of atrial fibrillation associated with these drugs is still low,” lead investigator Morten Schmidt (Aarhus University Hospital, Denmark) told heartwire . “The use of NSAIDs is associated with an increased risk, but overall the absolute risk is still small. Like any other drug, for physicians that prescribe NSAIDs it continues to be a question of balancing the benefits and risks.”

The study, published July 4, 2011 in the British Medical Journal, examined the risk of atrial fibrillation or flutter associated with NSAID use. It included 32 602 patients diagnosed with atrial fibrillation or flutter in Northern Denmark between 1999–2008 and 325 918 age- and gender-matched controls selected from the source population. Schmidt, a junior research fellow in the department of clinical epidemiology, said that a previous study had suggested that traditional NSAIDs were associated with an increased risk of atrial fibrillation in long-term users, and that one meta-analysis had indicated that COX-2 inhibitors, in particular rofecoxib (Vioxx, Merck & Co), also could be associated with cardiac arrhythmias, but no data specifically on atrial fibrillation were available before now.

Compared with controls who were not treated with the drugs, current use of nonselective NSAIDs was associated with an adjusted 17% increased risk of developing atrial fibrillation or flutter (incidence rate ratio [IRR] 1.17; 95% CI 1.10–1.24). Current use of COX-2 inhibitors was associated with a slightly higher risk of atrial fibrillation or flutter (IRR 1.27; 95% CI 1.20–1.34).

New use appeared to be associated with the highest risk of developing atrial fibrillation or flutter. For those who filled a first prescription for an NSAID or COX-2 inhibitor in the previous two months, there was a statistically significant 46% and 71% increased risk of atrial fibrillation/flutter, respectively, compared with controls not treated with the drugs.

“Atrial fibrillation and flutter needs to be considered when prescribing these drugs,” said Schmidt. “We did see a higher relative risk when using the COX-2 inhibitors compared with the nonselective NSAIDs, but as for the reason or mechanism behind this, we just don’t have any data on that right now.”

“A cautious approach”

In an accompanying editorial [2], Dr Jerry Gurwitz (University of Massachusetts Medical School, Worchester) said the findings have “important clinical and public health implications because of the high prevalence of use of these agents, particularly among older adults, and the increasing prevalence of atrial fibrillation with advancing age.”

However, Gurwitz notes that the present study found the highest risk among new users, whereas the UK database study found the highest risk among long-term users. In both trials, there was a lack of consistent dose-response with the drugs, making the association “even more tenuous.” Gurwitz also adds that case-control studies are subject to unmeasured confounding variables, such as obesity. In this analysis, Schmidt and colleagues were unable to obtain data on several clinical measures, including body mass index.

“What should clinicians do in practice in the light of current evidence?” asks the editorial. “With uncertainty regarding a plausible biological mechanism, the susceptibility of case-control studies to unmeasured confounders, and inconsistent results in the two studies performed to date, a cautious approach seems warranted in applying the study’s results to the care of patients.”

 

SmartPlanet.com, July 6, 2011  —  Are robotic vehicles the future of driving? Stanford University researchers think so. They’ve invented, Junior, a four-wheeled autonomous vehicle that drives just like a regular car, but without the need for a human operator. SmartPlanet looks at the internal systems behind Junior and how it’s able to sense obstacles, make turns, and avoid collisions.