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“Don’t Do, Because You Will Get Caught”

The American Society for Investigative Pathology hosted a very engaging and informational session on scientific integrity with regards to publishing, intellectual property and conflicts of interest. One might be inclined to think! Well! It’s my work, I should be able to do whatever I want with it Right? WRONG! The need for scientists to be innovative is becoming increasingly challenging! Scientist are now expected to publish more, seek alternative funding mechanisms and all the while discover ways to improve upon their respective research programs. Due to these new strains, it is not surprising to see the incidence of breeches in scientific integrity becoming more of a problem.

It is hard to determine where to draw the line when it comes to issues in scientific integrity. For example, if a principle investigator receives funding from a private institution, he/she may not be able to publish their data. Moreover, there are issues surrounding “Conflicts of Interest” or COI’s. Various questions can arise….Did you skew that data? Did you omit those results on purpose? Are the techniques you used proprietary, the list goes on and on. When you think about it, we all have our own conflicts of interest, but when it comes to the research setting, you better well make sure that you are handling things properly.

This lunch and learn session was engaging and also included the audience acting as a make shift jury, judging if the constituents and their actions were GUILTY or INNOCENT or ??, which means that topic is a tricky one . A case in scientific integrity was presented and covered various aspects listed below. Let’s just say there were very simple take home messages from each topic discussed and they are also included below.

Publishing

  1. Citation Bias and Reference Accuracy – “Actually read the citations you put in your paper. If something is inaccurate, you risk the chance of increasing that inaccuracy”
  2. Omitting negative results – “Everyone wants a beautiful research story, however if the data solidifies your results, please do not omit. Negative data can be IMPORTANT too geez”
  3. Redundant Data – “Okay people! Don’t try to change the title of your study and resubmit it to another journal or as a research grant, like it is new data”
  4. Plagiarism – “Plagiarism is plagiarism is plagiarism…point PERIOD!

Image Manipulation

  1. Image Scaling – “Add a scale to fluorescent and microscopy images of biological specimens; a good rule of thumb is to add the scale before enlarging the image.
  2. Microscope – “Imaging is NOT the microscope, it is the sample prep. Be sure control for the processing of your sample during its preparation.
  3. Pixilation – Anything that alters the pixels…..JUST STAY AWAY!

Conflicts of Interest

Ultimate take home message is, if you think you have a conflict of interest, it is most likely that you do. To avoid potential issues, you should contact your university’s conflict of interest office to minimize risk and substantiate yourself as a scientist who has integrity!

Remember to DO THE RIGHT THING! Remember that what you do now, does matter. In the process of understanding this complex world around us, make sure you do your due diligence to make those understandings easier. Try not to input your own personal biases and do your best to write with integrity!

“There is no such thing as a minor lapse of integrity” ― Tom Peters

April 27th, 2014 (11:45 AM – 1:45 PM ) – Experimental Biology 2014
XIVth Annual ASIP/AAA Career Development & Mentoring Program and Lunch: GUILTY Until Proven INNOCENT: Scientific Integrity and Getting Published!
 
San Diego Marriott Marquis & Marina, Presidio 
Chaired by Jayne Reuben , Titus Reaves , Jacqueline Jones-Triche 

@ASIPath, #xbio

The American Society for Investigative Pathology (ASIP) and the Boston Institute for Contemporary Art hosted a great event on last night! Here is my take on how art and science goes hand and hand!

“Stairways to a science Zenith”

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“This is what happens, when cells get board”

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“Clearly, this guy western blot didn’t work”

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“Bacilli can have fun too, see they reorient themselves”

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“When grad students leave their mark”

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“This is missing in every lab”

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“When professors show their creativity”

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#eb2013 #asipcentennial #boston

Last night the American Society for Investigative Pathology celebrated its 100th anniversary in a lavish, star studded gala at the Boston Institute for Contemporary Art. If you did not attend, then you missed out “Big Time”.  As a trainee, it was a great experience to be in the company of so many science greats. I sat a table with 3 past ASIP presidents, one who currently serves as the FASEB president. I like to think that I had the best table in the house!! Throughout the night, ASIP honored many of the society members, including the newest to the oldest members. The energy in the room was utterly amazing. The members of ASIP certainly displayed much pride for their organization. There was even a moment during the banquet when a question was asked: “How many society members have never received an ASIP award?”. To my amazement only two individuals raised their hands. That in and of itself is outstanding and admirable. It is clear that ASIP stands as not only just a science society, but a beacon of opportunity, fostering the careers of future trainees, while promoting excellence in science and camaraderie amongst scientists. I salute ASIP for its efforts and I have great expectations towards their contributions in the future.

Happy Centennial to the American Society for Investigative Pathology!

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#eb2013 #boston #asipcentennial

 

Okay!

No one told me how “interesting” it would be to get around in Boston. I am very thankful for the public transportation, however from the outside looking in, it can be somewhat scary at times. I did not realize the amount of effort I would need to take to get to my final destination; that being the Boston Convention and Exhibition Center. Despite my short journey, I must admit I have had a great time and it was a great chance to feel like a local and see the city. To be honest, I am quite proud of myself and I look forward to discovering more. So for a moment, I take a break from science and I give you something fun to view. The adventures of a lost scientist-in-training.  ENJOY!

“Never leave home without good traveling socks”

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“Standing on the streets of Boston”

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“It’s a beautiful day in the neighborhood”

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“Back Bay Station, my first stop”

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“A moment of silence for all the past locomotives”

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“After switching to the Sliver Line (Underground Bus ~ 5 mins) Bingo!! Final Destination (Boston Convention Center)”

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#eb2013, #ASIPcentennial

This year’s experimental biology meeting is being held in Boston, Massachusetts. It is no secret that the recent series of unfortunate events surrounding the Boston Marathon bombings has caused a dampening on this city’s morale. However, with the recent capture of the fugitives responsible, the city is now back to normal, after being on extreme lock down for the last several days.

There were several moments, in which I thought that the Experimental Biology 2013 meeting would not take place. But low and behold, the meeting is back on track (with increased security measures of course) and this great gathering of scientists is taking place at this very moment. Boston is stronger than ever and I look forward to exploring this wonderful city.  There is so much research, but oh so little time. Nevertheless follow me as I explore some of the most cutting edge research taking place right now. As the official meeting blogger for the American Society for Investigative Pathology (ASIP), we celebrate 100 years of science excellence.

Follow Along!!

Scireflector

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Either I’m nobody or I’m a NATION!

~Derek Walcott~

As the 2012 Experimental  Biology meeting comes to a close, I can not help but feel a sign of relief and disappointment. I am jaded in the sense that I will be leaving such a beautiful city, but also I am exhausted! However, I am a bit reluctant to err on the side of being happy that the meeting is over do to the fact that I had an absolute BLAST!

The following quote above comes from one of my favorite poets of all time; Derek Walcott is his name and let’s just say this Caribbean manipulator of prose sets the tone for this meeting’s close. So what in the world does this quote have to do with Experimental Biology 2012? Actually, that is a great question and I am so glad you asked!

Experimental Biology is one of the largest meetings in the world on science. It bridges multiple disciplines and brings people from all sorts of worldwide destinations to one big “geek fest”, a much needed and highly appreciated geek fest I must say! But, because the Experimental Biology meeting is so large, one might ponder on how their research contribution could mean anything amongst this vast array of science talent. For trainees this feeling comes more often than none! However, it is this very intricate culmination of a little here and there that makes EB such a great meeting.

As a new “kid on the block” in the blogging game, I salute all science bloggers who I have met on this trip and I am appreciative of your help! I’m not the type to give shout outs because I feel I might miss someone. But……. I have to give a huge shout out to Angela Hopp, (@angelahopp) , @scicurious, @hapsci, @DNLee5 for their media expertise and also the American Society for Investigative Pathology (@ASIPath).

Either I am a nobody stands to reaffirm us of our humility in this science game. It is healthy sometimes to not feel like you have it all together. I like to think it creates constant hunger and rejects complacency. However being a nobody doesn’t have to be a means to an end, because you could also “be a nation” and certainly when science appreciators come together for a meeting like this, that is exactly what we are.

A  science nation!!

 

 

 

Chronic fatigue syndrome, a medical disorder characterized by extreme and ongoing fatigue with no other diagnosed cause, remains poorly understood despite decades of scientific study. Although researchers estimate that more than 1 million Americans are affected by this condition, the cause for chronic fatigue syndrome, a definitive way to diagnose it, and even its very existence remain in question. In a new study, researchers have found differing brain responses in people with this condition compared to healthy controls, suggesting an association between a biologic functional response and chronic fatigue syndrome.

The findings show that patients with chronic fatigue syndrome have decreased activation of an area of the brain known as the basal ganglia in response to reward. Additionally, the extent of this lowered activation was associated with each patient’s measured level of fatigue. The basal ganglia are at the base of the brain and are associated with a variety of functions, including motor activity and motivation. Diseases affecting basal ganglia are often associated with fatigue. These results shed more light on this mysterious condition, information that researchers hope may eventually lead to better treatments for chronic fatigue syndrome.

The study was conducted by Elizabeth R. Unger, James F. Jones, and Hao Tian of the Centers for Disease Control and Prevention (CDC), Andrew H. Miller and Daniel F. Drake of Emory University School of Medicine, and Giuseppe Pagnoni of the University of Modena and Reggio Emilia. An abstract of their study entitled, “Decreased Basal Ganglia Activation in Chronic Fatigue Syndrome Subjects is Associated with Increased Fatigue,” will be discussed at the meeting Experimental Biology 2012, being held April 21-25 at the San Diego Convention Center. The abstract is sponsored by the American Society for Investigative Pathology (ASIP), one of six scientific societies sponsoring the conference which last year attracted some 14,000 attendees.

More Fatigue, Less Activation
Dr. Unger says that she and her colleagues became curious about the role of the basal ganglia after previous studies by collaborators at Emory University showed that patients treated with interferon alpha, a common treatment for chronic hepatitis C and several other conditions, often experienced extreme fatigue. Further investigation into this phenomenon showed that basal ganglia activity decreased in patients who received this immune therapy. Since the fatigue induced by interferon alpha shares many characteristics with chronic fatigue syndrome, Unger and her colleagues decided to investigate whether the basal ganglia were also affected in this disorder.

The researchers recruited 18 patients with chronic fatigue syndrome, as well as 41 healthy volunteers with no symptoms of CFS. Each study participant underwent functional magnetic resonance imaging, a brain scan technique that measures activity in various parts of the brain by blood flow, while they played a simple card game meant to stimulate feelings of reward. The participants were each told that they’d win a small amount of money if they correctly guessed whether a preselected card was red or black. After making their choice, they were presented with the card while researchers measured blood flow to the basal ganglia during winning and losing hands.

The researchers showed that patients with chronic fatigue syndrome experienced significantly less change in basal ganglia blood flow between winning and losing than the healthy volunteers. When the researchers looked at scores for the Multidimensional Fatigue Inventory, a survey often used to document fatigue for chronic fatigue syndrome and various other conditions, they also found that the extent of a patient’s fatigue was tightly tied with the change in brain activity between winning and losing. Those with the most fatigue had the smallest change.

Results Suggest Role of Inflammation
Unger notes that the findings add to our understanding of biological factors that may play a role in chronic fatigue syndrome. “Many patients with chronic fatigue syndrome encounter a lot of skepticism about their illness,” she says. “They have difficulty getting their friends, colleagues, coworkers, and even some physicians to understand their illness. These results provide another clue into the biology of chronic fatigue syndrome.”

The study also suggests some areas of further research that could help scientists develop treatments for this condition in the future, she adds. Since the basal ganglia use the chemical dopamine as their major neurotransmitter, dopamine metabolism may play an important role in understanding and changing the course of this illness. Similarly, the difference in basal ganglia activation between the patients and healthy volunteers may be caused by inflammation, a factor now recognized as pivotal in a variety of conditions, ranging from heart disease to cancer.

Estimates from the CDC suggest that annual medical costs associated with chronic fatigue syndrome total about $14 billion in the United States. Annual losses to productivity because of lost work time range between $9 and $37 billion, with costs to individual households ranging between $8,000 and $20,000 per year.

Adapted from Donna Krupa (dkrupa@the-aps.org)

Researchers are constantly searching for methods to generate models for testing hypotheses within the context of biological relevance. Not only is it important to generate models that are fully functional to test an hypothesis, but these models must mimic that biological system of interest as seen within its natural context. Scientists at the University of Leipzig in Germany are lending their expertise in this emerging area with particular focus on the liver. The liver plays a variety of very pivotal roles in the human body, such as detoxifying drugs and other substances that we ingest,  protein synthesis and fat metabolism.

Primary hepatocytes (liver cells) present an appropriate model for the validation of a system for toxicological studies of new drugs and chemicals that may be used in the pharmaceutical/cosmetics industries and biologically relevant models are needed to test the affects of these chemicals within a biological context. However, there are no models currently available to do this.

Dr. Peggy Stock and her colleagues at the University of Leipzig in Germany are conducting research in generating appropriate models for liver toxicity studies. In preliminary studies presented at the 2012 Experimental Biology Conference in San Diego, California, this group presented data analysing the applicability of using 3D versus 2D collagen-coated silicone scaffolds for models of human liver. This group utilized rat hepatocytes (rat liver cells) as a cellular model for human liver, since rat liver cell processes mimic that of humans to a high degree.

Primary rat hepatocytes were cultured (grown) for 72h on a 3D structure and was compared with 2D culture on conventional cell culturing methods utilizing cell culture dishes. Cell counts and the growth patterns of these cells on silicone and the urea production rate were also determined as urea production takes place in the liver and it can serve as a marker of liver health and function.

Based on identical initial cell counts the growth rate was about 42% higher in 3D culture as compared to 2D. In addition, cells attached to the scaffold and formed clusters and organ-like structures that are native to the liver. The 3D culture on the silicone scaffold displayed no significant signs of toxicity after 3 days of cell culture. The urea production rate, which is a marker of liver health and function, was significantly higher in the 3D vs 2D cell culturing system.

Results from these studies demonstrate the appropriateness of using 3D models for the culture of primary rat hepatocytes. Thus, revealing that these 3D scaffolds may be utilized as an important tool for the development of 3D liver models for understanding and examining liver function within a laboratory setting.

Results of study using animal model among the presentations at the meeting
Experimental Biology 2012

SAN DIEGO— Heart failure is the most common cause of death throughout the world, typically the result of chronic high blood pressure, also known as hypertension. As a result, research efforts have focused on an array of approaches aimed at preventing and treating high blood pressure. Recently, Japanese researchers examined the utility of an anti-hypertensive drug, moxonidine, which acts on the imidazoline receptors in the cardiovascular center of the brainstem. They found, using an animal model, that the drug can improve heart function and survival independent of its effect on blood pressure. They also found the drug had a favorable effect on oxidative stress, which is related to insulin resistance, the underlying abnormality in diabetes, which is common in people with heart failure.

An abstract presentation about the findings will be offered at the meeting Experimental Biology 2012, being held April 21-25 at the San Diego Convention Center. The study was conducted by Yoshitaka Hirooka, Nobuhiro Honda, Ryuichi Matsukawa, Koji Itou and Kenji Sunagawa, all of the Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences in Fukuoka, Japan. It is entitled, “Central sympathoinibition improves left ventricular function during the transition from hypertrophy to heart failure in Dahl salt-sensitive rats.” The abstract is sponsored by the American Society for Investigative Pathology (ASIP), one of six scientific societies sponsoring the conference which last year attracted some 14,000 attendees.

Heart failure is a chronic disease that takes many forms and a variety of medications are used to treat it. Drugs such as ACE inhibitors and beta blockers target the causes of systolic heart failure. Clonidine, a first-generation central sympathoinhibitory drug, targets brain receptors that reduce cardiac output and lower blood pressure. Moxonidine, a second-generation drug, targets diastolic heart failure and function by reducing the effect of the central nervous system (CNS) receptors to decrease sympathetic activation and thus reduce blood pressure. In the study, salt-sensitive, hypertensive rats either received Moxonidine or were assigned to the control group. Researchers later found that the animals who received the drug had a marked inhibition of the sympathetic activity (an area of the brain) compared to those that did not. The findings suggest that inhibition of the central sympathetic outflow is important in the mechanism of hypertension. According to Dr. Hirooka, “The findings are important because they suggest that moxonidine may be useful in targeting the central receptors in the brain that are known to occur in patients with hypertension.”

Next Steps
The study is the latest in a series conducted by the research team whose focus is on neural control of circulation in hypertension and heart failure. Looking ahead, they will work to identify the precise mechanisms involved in the beneficial effect of moxonidine, Dr. Hirooka said. They will also study other ways to see if the compound is a possible therapeutic tool for hypertensive heart disease to prevent heart failure. As the drug had beneficial effects on insulin resistance, they would like to further investigate the issue, he added Maxonidine is available in select countries in Europe and Asia. It is not currently available in the United States.

Adapted from Donna Kupa (dkrupa@the-aps.org)