Advertisements
Feeds:
Posts
Comments

Archive for the ‘Population Health Management’ Category


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Scientists at the Stanford University School of Medicine have completed the first-ever characterization of the meticulously timed immune system changes in women that occur during pregnancy. The findings were published in Science Immunology revealed that there is an immune clock of pregnancy and suggest it may help doctors predict preterm birth.

 

The timing of immune system changes follows a precise and predictable pattern in normal pregnancy. Although physicians have long known that the expectant mother’s immune system adjusts to prevent her body from rejecting the fetus, no one had investigated the full scope of these changes, nor asked if their timing was tightly controlled.

 

Nearly 10 percent of U.S. infants are born prematurely, arriving three or more weeks early, but physicians lack a reliable way to predict premature deliveries. Previous research at Stanford and other places suggested that inflammatory immune responses may help in triggering early labor. It suggested that if scientists identify an immune signature of impending preterm birth, they should be able to design a blood test to detect it.

 

The researchers used mass cytometry, a technique developed at Stanford, to simultaneously measure up to 50 properties of each immune cell in the blood samples. They counted the types of immune cells, assessed what signaling pathways were most active in each cell, and determined how the cells reacted to being stimulated with compounds that mimic infection with viruses and bacteria.

 

The researchers developed an algorithm that captures the immunological timeline during pregnancy that both validates previous findings and sheds new light on immune cell interaction during gestation. By defining this immunological chronology during normal term pregnancy, they can now begin to determine which alterations associate with pregnancy-related pathologies.

 

With an advanced statistical modeling technique, introduced for the first time in this study, the scientists then described in detail how the immune system changes throughout pregnancy. Instead of grouping the women’s blood samples by trimester for analysis, the model treated gestational age as a continuous variable, allowing the researchers to account for the exact time during pregnancy at which each sample was taken. The mathematical model also incorporated knowledge from the existing scientific literature of how immune cells behave in nonpregnant individuals to help determine which findings were most likely to be important.

 

The study confirmed immune features of pregnancy that were already known. Such as the scientists saw that natural killer cells and neutrophils have enhanced action during pregnancy. The researchers also uncovered several previously unappreciated features of how the immune system changes, such as the finding that activity of the STAT5 signaling pathway in CD4+T cells progressively increases throughout pregnancy on a precise schedule, ultimately reaching levels much higher than in nonpregnant individuals. The STAT5 pathway is involved in helping another group of immune cells, regulatory T cells, to differentiate. Interestingly, prior research in animals has indicated that regulatory T cells are important for maintaining pregnancy.

 

The next step will be to conduct similar research using blood samples from women who deliver their babies prematurely to see where their trajectories of immune function differ from normal.

 

This study revealed a precisely timed chronology of immune adaptations in peripheral blood over the course of a term pregnancy. This finding was enabled by high-content, single-cell mass cytometry coupled with a csEN algorithm accounting for the modular structure of the immune system and previous knowledge. The study provided the conceptual backbone and the analytical framework to examine whether disruption of this chronology is a diagnostically useful characteristic of preterm birth and other pregnancy-related pathologies.

 

References:

 

http://immunology.sciencemag.org/content/2/15/eaan2946.full

 

http://med.stanford.edu/news/all-news/2017/09/immune-system-changes-during-pregnancy-are-precisely-timed.html

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078586/

 

http://www.nature.com/nm/journal/v19/n5/full/nm.3160.html?foxtrotcallback=true

 

https://www.ncbi.nlm.nih.gov/pubmed/14758358

Advertisements

Read Full Post »


Decline in Sperm Count – Epigenetics, Well-being and the Significance for Population Evolution and Demography

 

Dr. Marc Feldman, Expert Opinion on the significance of Sperm Count Decline on the Future of Population Evolution and Demography

Dr. Sudipta Saha, Effects of Sperm Quality and Quantity on Human Reproduction

Dr. Aviva Lev-Ari, Psycho-Social Effects of Poverty, Unemployment and Epigenetics on Male Well-being, Physiological Conditions affecting Sperm Quality and Quantity

 

Recent studies concluded via rigorous and comprehensive analysis found that Sperm Count (SC) declined 52.4% between 1973 and 2011 among unselected men from western countries, with no evidence of a ‘leveling off’ in recent years. Declining mean SC implies that an increasing proportion of men have sperm counts below any given threshold for sub-fertility or infertility. The high proportion of men from western countries with concentration below 40 million/ml is particularly concerning given the evidence that SC below this threshold is associated with a decreased monthly probability of conception.

1.Temporal trends in sperm count: a systematic review and meta-regression analysis 

Hagai Levine, Niels Jørgensen, Anderson Martino‐Andrade, Jaime Mendiola, Dan Weksler-Derri, Irina Mindlis, Rachel Pinotti, Shanna H SwanHuman Reproduction Update, July 25, 2017, doi:10.1093/humupd/dmx022.

Link: https://academic.oup.com/humupd/article-lookup/doi/10.1093/humupd/dmx022.

2. Sperm Counts Are Declining Among Western Men – Interview with Dr. Hagai Levine

https://news.afhu.org/news/sperm-counts-are-declining-among-western-men?utm_source=Master+List&utm_campaign=dca529d919-EMAIL_CAMPAIGN_2017_07_27&utm_medium=email&utm_term=0_343e19a421-dca529d919-92801633

3. Trends in Sperm Count – Biological Reproduction Observations

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

4. Long, mysterious strips of RNA contribute to low sperm count – Long non-coding RNAs can be added to the group of possible non-structural effects, possibly epigenetic, that might regulate sperm counts.

http://casemed.case.edu/cwrumed360/news-releases/release.cfm?news_id=689

https://scienmag.com/long-mysterious-strips-of-rna-contribute-to-low-sperm-count/

Dynamic expression of long non-coding RNAs reveals their potential roles in spermatogenesis and fertility

Published: 29 July 2017
Thus, we postulated that some lncRNAs may also impact mammalian spermatogenesis and fertility. In this study, we identified a dynamic expression pattern of lncRNAs during murine spermatogenesis. Importantly, we identified a subset of lncRNAs and very few mRNAs that appear to escape meiotic sex chromosome inactivation (MSCI), an epigenetic process that leads to the silencing of the X- and Y-chromosomes at the pachytene stage of meiosis. Further, some of these lncRNAs and mRNAs show strong testis expression pattern suggesting that they may play key roles in spermatogenesis. Lastly, we generated a mouse knock out of one X-linked lncRNA, Tslrn1 (testis-specific long non-coding RNA 1), and found that males carrying a Tslrn1 deletion displayed normal fertility but a significant reduction in spermatozoa. Our findings demonstrate that dysregulation of specific mammalian lncRNAs is a novel mechanism of low sperm count or infertility, thus potentially providing new biomarkers and therapeutic strategies.

This article presents two perspectives on the potential effects of Sperm Count decline.

One Perspective identifies Epigenetics and male well-being conditions

  1. as a potential explanation to the Sperm Count decline, and
  2. as evidence for decline in White male longevity in certain geographies in the US since the mid 80s.

The other Perspective, evaluates if Sperm Count Decline would have or would not have a significant long term effects on Population Evolution and Demography.

The Voice of Prof. Marc Feldman, Stanford University – Long term significance of Sperm Count Decline on Population Evolution and Demography

Poor sperm count appears to be associated with such demographic statistics as life expectancy (1), infertility (2), and morbidity (3,4). The meta-analysis by Levine et al. (5) focuses on the change in sperm count of men from North America, Europe, Australia, and New Zealand, and shows a more than 50% decline between 1973 and 2011. Although there is no analysis of potential environmental or lifestyle factors that could contribute to the estimated decline in sperm count, Levine et al. speculate that this decline could be a signal for other negative changes in men’s health.

Because this study focuses mainly on Western men, this remarkable decline in sperm count is difficult to associate with any change in actual fertility, that is, number of children born per woman. The total fertility rate in Europe, especially Italy, Spain, and Germany, has slowly declined, but age at first marriage has increased at the same time, and this increase may be more due to economic factors than physiological changes.

Included in Levine et al.’s analysis was a set of data from “Other” countries from South America, Asia, and Africa. Sperm count in men from these countries did not show significant trends, which is interesting because there have been strong fertility declines in Asia and Africa over the same period, with corresponding increases in life expectancy (once HIV is accounted for).

What can we say about the evolutionary consequences for humans of this decrease? The answer depends on the minimal number of sperm/ml/year that would be required to maintain fertility (per woman) at replacement level, say 2.1 children, over a woman’s lifetime. Given the smaller number of ova produced per woman, a change in the ovulation statistics of women would be likely to play a larger role in the total fertility rate than the number of sperm/ejaculate/man. In other words, sperm count alone, absent other effects on mortality during male reproductive years, is unlikely to tell us much about human evolution.

Further, the major declines in fertility over the 38-year period covered by Levine et al. occurred in China, India, and Japan. Chinese fertility has declined to less than 1.5 children per woman, and in Japan it has also been well below 1.5 for some time. These declines have been due to national policies and economic changes, and are therefore unlikely to signal genetic changes that would have evolutionary ramifications. It is more likely that cultural changes will continue to be the main drivers of fertility change.

The fastest growing human populations are in the Muslim world, where fertility control is not nearly as widely practiced as in the West or Asia. If this pattern were to continue for a few more generations, the cultural evolutionary impact would swamp any effects of potentially declining sperm count.

On the other hand, if the decline in sperm count were to be discovered to be associated with genetic and/or epigenetic phenotypic effects on fetuses, newborns, or pre-reproductive humans, for example, due to stress or obesity, then there would be cause to worry about long-term evolutionary problems. As Levine et al. remark, “decline in sperm count might be considered as a ‘canary in the coal mine’ for male health across the lifespan”. But to date, there is little evidence that the evolutionary trajectory of humans constitutes such a “coal mine”.

References

  1. Jensen TK, Jacobsen R, Christensen K, Nielsen NC, Bostofte E. 2009. Good semen quality and life expectancy: a cohort study of 43,277 men. Am J Epidemiol 170: 559-565.
  2. Eisenberg ML, Li S, Behr B, Cullen MR, Galusha D, Lamb DJ, Lipshultz LI. 2014. Semen quality, infertility and mortality in the USA. Hum Reprod 29: 1567-1574.
  3. Eisenberg ML, Li S, Cullen MR, Baker LC. 2016. Increased risk of incident chronic medical conditions in infertile men: analysis of United States claims data. Fertil Steril 105: 629-636.
  4. Latif T, Kold Jensen T, Mehlsen J, Holmboe SA, Brinth L, Pors K, Skouby SO, Jorgensen N, Lindahl-Jacobsen R. Semen quality is a predictor of subsequent morbidity. A Danish cohort study of 4,712 men with long-term follow-up. Am J Epidemiol. Doi: 10.1093/aje/kwx067. (Epub ahead of print]
  5. Levine H, Jorgensen N, Martino-Andrade A, Mendiola J, Weksler-Derri D, Mindlis I, Pinotti R, Swan SH. 2017. Temporal trends in sperm count: a systematic review and meta-regression analysis. Hum Reprod Update pp. 1-14. Doi: 10.1093/humupd/dmx022.

SOURCE

From: Marcus W Feldman <mfeldman@stanford.edu>

Date: Monday, July 31, 2017 at 8:10 PM

To: Aviva Lev-Ari <aviva.lev-ari@comcast.net>

Subject: Fwd: text of sperm count essay

Psycho-Social Effects of Poverty, Unemployment and Epigenetics on Male Well-being, Physiological Conditions as POTENTIAL effects on Sperm Quality and Quantity and Evidence of its effects on Male Longevity

The Voice of Carol GrahamSergio Pinto, and John Juneau II , Monday, July 24, 2017, Report from the Brookings Institute

  1. The IMPACT of Well-being, Stress induced by Worry, Pain, Perception of Hope related to Employment and Lack of employment on deterioration of Physiological Conditions as evidence by Decrease Longevity

  2. Epigenetics and Environmental Factors

The geography of desperation in America

Carol GrahamSergio Pinto, and John Juneau II Monday, July 24, 2017, Report from the Brookings Institute

In recent work based on our well-being metrics in the Gallup polls and on the mortality data from the Centers for Disease Control and Prevention, we find a robust association between lack of hope (and high levels of worry) among poor whites and the premature mortality rates, both at the individual and metropolitan statistical area (MSA) levels. Yet we also find important differences across places. Places come with different economic structures and identities, community traits, physical environments and much more. In the maps below, we provide a visual picture of the differences in in hope for the future, worry, and pain across race-income cohorts across U.S. states. We attempted to isolate the specific role of place, controlling for economic, socio-demographic, and other variables.

One surprise is the low level of optimism and high level of worry in the minority dense and generally “blue” state of California, and high levels of pain and worry in the equally minority dense and “blue” states of New York and Massachusetts. High levels of income inequality in these states may explain these patterns, as may the nature of jobs that poor minorities hold.

We cannot answer many questions at this point. What is it about the state of Washington, for example, that is so bad for minorities across the board? Why is Florida so much better for poor whites than it is for poor minorities? Why is Nevada “good” for poor white optimism but terrible for worry for the same group? One potential issue—which will enter into our future analysis—is racial segregation across places. We hope that the differences that we have found will provoke future exploration. Readers of this piece may have some contributions of their own as they click through the various maps, and we welcome their input. Better understanding the role of place in the “crisis” of despair facing our country is essential to finding viable solutions, as economic explanations, while important, alone are not enough.

https://www.brookings.edu/research/the-geography-of-desperation-in-america/?utm_medium=social&utm_source=facebook&utm_campaign=global

 

Read Full Post »


Trends in Sperm Count

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

There has been a genuine decline in semen quality over the past 50 years. There is lot of controversy about this as there are limitations in studies that have attempted to address it. Sperm count is of considerable public health importance for several reasons. First, sperm count is closely linked to male fecundity and is a crucial component of semen analysis, the first step to identify male factor infertility.

Reduced sperm count is associated with cryptorchidism, hypospadias and testicular cancer. It may be associated with multiple environmental influences, including endocrine disrupting chemicals, pesticides, heat and lifestyle factors, including diet, stress, smoking and BMI. Therefore, sperm count may sensitively reflect the impacts of the modern environment on male health throughout the life span.

This study provided a systematic review and meta-regression analysis of recent trends in sperm counts as measured by sperm concentration (SC) and total sperm count (TSC), and their modification by fertility and geographic group. Analyzing trends by birth cohorts instead of year of sample collection may aid in assessing the causes of the decline (prenatal or in adult life) but was not feasible owing to lack of information.

This rigorous and comprehensive analysis found that SC declined 52.4% between 1973 and 2011 among unselected men from western countries, with no evidence of a ‘leveling off’ in recent years. Declining mean SC implies that an increasing proportion of men have sperm counts below any given threshold for sub-fertility or infertility. The high proportion of men from western countries with concentration below 40 million/ml is particularly concerning given the evidence that SC below this threshold is associated with a decreased monthly probability of conception.

Declines in sperm count have implications beyond fertility and reproduction. The decline reported in this study is consistent with reported trends in other male reproductive health indicators, such as testicular germ cell tumors, cryptorchidism, onset of male puberty and total testosterone levels. The public health implications are even wider. Recent studies have shown that poor sperm count is associated with overall morbidity and mortality. While the current study is not designed to provide direct information on the causes of the observed declines, sperm count has been plausibly associated with multiple environmental and lifestyle influences, both prenatally and in adult life. In particular, endocrine disruption from chemical exposures or maternal smoking during critical windows of male reproductive development may play a role in prenatal life, while lifestyle changes and exposure to pesticides may play a role in adult life.

These findings strongly suggest a significant decline in male reproductive health, which has serious implications beyond fertility concerns. Research on causes and implications of this decline is urgently needed.

 

REFERENCES

Temporal trends in sperm count: a systematic review and meta-regression analysis 

Hagai Levine, Niels Jørgensen, Anderson Martino‐Andrade, Jaime Mendiola, Dan Weksler-Derri, Irina Mindlis, Rachel Pinotti, Shanna H Swan. Human Reproduction Update, July 25, 2017, doi:10.1093/humupd/dmx022.

Link: https://academic.oup.com/humupd/article-lookup/doi/10.1093/humupd/dmx022.

Sperm Counts Are Declining Among Western Men – Interview with Dr. Hagai Levine

https://news.afhu.org/news/sperm-counts-are-declining-among-western-men?utm_source=Master+List&utm_campaign=dca529d919-EMAIL_CAMPAIGN_2017_07_27&utm_medium=email&utm_term=0_343e19a421-dca529d919-92801633

J Urol. 1983 Sep;130(3):467-75.

A critical method of evaluating tests for male infertility.

https://www.ncbi.nlm.nih.gov/pubmed/6688444

Hum Reprod. 1993 Jan;8(1):65-70.

Estimating fertility potential via semen analysis data.

https://www.ncbi.nlm.nih.gov/pubmed/8458929

Lancet. 1998 Oct 10;352(9135):1172-7.

Relation between semen quality and fertility: a population-based study of 430 first-pregnancy planners.

https://www.ncbi.nlm.nih.gov/pubmed/9777833

Hum Reprod Update. 2010 May-Jun;16(3):231-45. doi: 10.1093/humupd/dmp048. Epub 2009 Nov 24.

World Health Organization reference values for human semen characteristics.

https://www.ncbi.nlm.nih.gov/pubmed/19934213

J Nutr. 2016 May;146(5):1084-92. doi: 10.3945/jn.115.226563. Epub 2016 Apr 13.

Intake of Fruits and Vegetables with Low-to-Moderate Pesticide Residues Is Positively Associated with Semen-Quality Parameters among Young Healthy Men.

https://www.ncbi.nlm.nih.gov/pubmed/27075904

Reprod Toxicol. 2003 Jul-Aug;17(4):451-6.

Semen quality of Indian welders occupationally exposed to nickel and chromium.

https://www.ncbi.nlm.nih.gov/pubmed/12849857

Fertil Steril. 1996 May;65(5):1009-14.

Semen analyses in 1,283 men from the United States over a 25-year period: no decline in quality.

https://www.ncbi.nlm.nih.gov/pubmed/8612826

Read Full Post »


The Rutgers Global Health Institute, part of Rutgers Biomedical and Health Sciences, Rutgers University, New Brunswick, New Jersey – A New Venture Designed to Improve Health and Wellness Globally  

Author: Gail S. Thornton, M.A.

Co-Editor: The VOICES of Patients, Hospital CEOs, HealthCare Providers, Caregivers and Families: Personal Experience with Critical Care and Invasive Medical Procedures

 

The newly formed Rutgers Global Health Institute, part of Rutgers Biomedical and Health Sciences (RBHS) of Rutgers University, New Brunswick, New Jersey (http://rbhs.rutgers.edu/), represents a new way of thinking by providing positive health outcomes to potential patients around the world affected by disease and/or by a negative environmental impact. The goal of the Institute is three-fold:

  • to improve the health and wellness of individuals and populations around the world,
  • to create a healthier world through innovation, engineering, and technology, and
  • to educate involved citizens and effective leaders in global health.

Richard G. Marlink, M.D., a former Harvard University professor recognized internationally for research and leadership in the fight against AIDS, was recently appointed as the inaugural Henry Rutgers Professor of Global Health and Director of the Rutgers Global Health Institute.

The Rutgers Global Health Institute was formed last year after research by the University into the most significant health issues affecting under-served and under-developed populations. While conducting research for its five-year strategic plan, the RBHS looked for bold and ambitious ways that they could take advantage of the changing health care environment and band together to tackle the world’s leading health and environmental causes, contributing to the betterment of society. One of the results was the formation of the Rutgers Global Health Institute, supporting cross-functionally Rutgers faculty, scientists, and clinicians who represent the best in their respective fields of health innovation, research and patient care related to global health.

More broadly, the RBHS, created in 2013, is one of the nation’s leading – and largest — academic health centers that provides health care education, research and clinical service and care. It is an umbrella organization that encompasses eight schools – Ernest Mario School of Pharmacy, Graduate School of Biomedical Sciences, New Jersey Medical School, Robert Wood Johnson Medical School, Rutgers School of Dental Medicine, School of Health Professions, School of Nursing and School of Public Health.

In addition, the RBHS encompasses six centers and institutes that provide cancer treatment and research, neuroscience, advanced biotechnology and medicine, environmental and occupational health and health care policy and aging research. Those centers and institutes are the Brain Health Institute, Center for Advanced Biotechnology and Medicine, Environmental and Occupational Health Sciences Institute, Institute for Health, Health Care Policy and Aging Research, Rutgers Cancer Institute of New Jersey, and Rutgers Institute for Translational Medicine and Research. And lastly, the RBHS includes the University Behavioral Health Care.

 

Rutgers Institute For Health Building

Image SOURCE: Photograph courtesy of the Rutgers Global Health Institute, Rutgers Biomedical and Health Sciences, Rutgers University, New Brunswick, New Jersey.   

 

Below is my interview with the Inaugural Henry Rutgers Professor of Global Health and Director of the Rutgers Global Health Institute Richard G. Marlink, M.D., which occurred in April, 2017.

You were recently appointed as the inaugural Henry Rutgers Professor of Global Health and Director of the new Rutgers Global Health Institute at Rutgers Biomedical and Health Sciences (RBHS). What are the goals of the new Institute?

Dr. Marlink: The overarching goal of the Rutgers Global Health Institute is to improve the health and wellness of individuals and populations in need both here and around the world, to create a healthier world through innovation, engineering, and technology, and to educate involved citizens and effective leaders in global health. We will do that by building on the aspiration of our originating organization — RBHS, which is to be recognized as one of the best academic health centers in the U.S., known for its education, research, clinical care, and commitment to improving access to health care and reducing health care disparities.

As the newly formed Rutgers Global Health Institute, we are embarking on an ambitious agenda to take advantage of the changing health care environment. Working across schools and disciplines at Rutgers University, we plan to have a significant impact within at least four signature programs identified by RBHS, which are cancer, environmental and occupational health, infection and inflammation, and public health. We also will include all other parts of Rutgers, as desired, beyond RBHS.

My background as a global health researcher, physician, and leader of grassroots health care delivery will help develop programs to undertake global health initiatives that assist populations locally and around the world. I believe that involved citizens, including students, can greatly impact major societal issues.

A key role in the strategic growth of Rutgers Biomedical and Health Sciences – an umbrella organization for eight schools, four centers and institutes and a behavioral health network — is to broaden the Rutgers University’s presence in the public health community globally to improve health and wellness. How will the new Rutgers Global Health Institute be part of this growth?

Dr. Marlink: Our RBHS Chancellor Brian Strom [M.D., M.P.H.] believes that we are positioned to become one of the finest research universities in the country, working cross-functionally with our three campuses in Newark, Camden and New Brunswick. In developing the strategic plan, Dr. Strom notes that we become much stronger and more capable and productive by leveraging our strengths to collaborate and working together across disciplines to best serve the needs of our community locally and globally.

Specifically, we are formulating plans to focus on these areas: old and new infectious disease epidemics; the expanding burden of noncommunicable diseases in poor populations; the social and environmental threats to health, poverty and humanitarian crises; and inadequate local and developing country health systems. We will support the development of global health research programs university-wide, the recruitment of faculty with interests in global health, and the creation of a web-based global health resource center for faculty and students with interests in these areas.

We are still a very young part of RBHS, and of Rutgers overall, so our plans are a work in progress. As tangible examples of our commitment to improving health and wellness globally, we plan to enhance global public health by establishing links between global public health and environmental and occupational health faculty in studies related to air pollution, climate change, and pesticide health.

Another example the Institute has in the works is expanding links with the School of Engineering. In fact, we are creating a senior-level joint faculty position with the School of Engineering and Rutgers-New Brunswick. Still other plans involve forging collaborative relationships between the Rutgers Cancer Program, under the auspices of Rutgers Cancer Institute of New Jersey, which is New Jersey’s only National Cancer Institute (NCI)-designated comprehensive cancer center, and other organizations and partners around the world, especially in poor and less-developed countries.

How is the Rutgers Global Health Institute strategically prepared for changing the health care paradigm?

Dr. Marlink: We intend to be an international global health leader in the health sciences, in public health, and in other related, but non-biomedical professions. This means that we will incorporate our learnings from laboratory sciences and the clinical, behavioral, and public health sciences, as well as from engineering, business, economics, law, and social sciences. This broad approach is critical in this health care environment as accountability for patient care is shifting to large groups of providers. Health care will be more value-driven and our health care teams must work collaboratively to be innovative. Our focus on health care is now also population-based, rather than only individual-based, and we are moving from large regional centers toward community centers, even in small and remote areas of the world. We are encouraged by rapid changes in technology that will provide new opportunities for shared knowledge, patient care and research.

Additionally, we are exploring ways to identify and recruit key faculty who will increase our breadth and depth of key disease areas as well as provide guidance on how to pursue science grants from the National Institute of Health (NIH)-funded program project grants and specialized research programs.

Currently, Rutgers University receives NIH funding for research in public health, population health, health promotion, wellness, health behavior, preventive medicine, and global health.

As a researcher, scholar and leader of grassroots health care delivery, how have your past positions prepared you for this new challenge? Your last position was the Bruce A. Beal, Robert L. Beal, and Alexander S. Beal Professor of the Practice of Public Health at Harvard University’s T.H. Chan School of Public Health and Executive Director of the Harvard AIDS Initiative.

Dr. Marlink: I have been a global health practitioner, researcher, and executive leader for almost three decades. I am trained in medical oncology and HIV medicine and have conducted clinical, epidemiological and implementation research in Africa since 1985. I was first introduced to global health when finishing my Hematology/Oncology fellowship at what is now the Beth Israel Deaconess Medical Center in the mid-1980’s in Boston.

During my Hematology/Oncology fellowship and after the co-organizing the first, hospital-based AIDS care clinic in the New England region, I was trying to learn the ropes in virology and molecular biology in the laboratory group of Max Essex at Harvard University. During that time in the mid-1980s, our laboratory group along with Senegalese and French collaborators discovered the first evidence for the existence of a new human retrovirus, HIV-2, a distinct second type of human AIDS virus, with its apparent origins in West Africa.

As a clinician, I was able to assist in Senegal, helping set up clinical care and create a research cohort in Dakar for hundreds of women sex workers infected with this new human retrovirus and care for them and their families. I discovered that a little can go a long way in poor settings, such as in Senegal. I became hooked on helping create solutions to help people in poor settings in Africa and elsewhere. Long-term partnerships and friendships have subsequently been made in many developing countries. Throughout my career, I have built successful partnerships with many governments, companies, and non-profit organizations, and those relationships have been the foundation to build successful public health partnerships in poor regions of the world.

In the 1990s, I helped create the Botswana-Harvard Partnership for HIV Research and Education (BHP). Through this partnership, the Government of Botswana and BHP have worked together to combat the AIDS epidemic in Botswana. Under my direction, and in partnership with the Botswana Ministry of Health, BHP launched the KITSO AIDS Training Program in 1999. Kitso is the Setswana word for ‘knowledge.”

KITSO is the national training program for physicians, nurses, and pharmacists, which has trained more than 14,000 health professionals in HIV/AIDS care and antiretroviral treatment. KITSO training modules address issues, such as antiretroviral therapy, HIV/AIDS-related disease management, gender-specific HIV issues, task-sharing, supportive and palliative care, and various psychosocial and counseling themes.

In addition, I was the Botswana County Director for Harvard Chan School’s 3-country President’s Emergency Plan AIDS Relief (PEPFAR) grant, The Botswana PEPFAR effort includes a Clinical and Laboratory Master Training Program and the creation of the Botswana Ministry of Health’s Monitoring and Evaluation Unit. Concurrently, I was the Principal Investigator of Project HEART in five African countries with the Elizabeth Glaser Pediatric AIDS Foundation.

Also in Botswana, in 2000, I was a co-founder of a distinct partnership involving a large commitment to the Government of Botswana from the Bill and Melinda Gates and Merck Foundations.  This commitment continues as an independent non-governmental organization (NGO) to provide support for various AIDS prevention and care efforts in Botswana and the region.

All these global health experiences, it seems, have led me to my new role at the Rutgers Global Health Institute.

What is your advice for ways that the business community or university students can positively impact major societal issues?

Dr. Marlink: My advice is to be optimistic and follow that desire to want to make a difference. Margaret Mead, the American cultural anthropologist, said years ago, “Never doubt that a small group of thoughtful, committed citizens can change the world; indeed, it’s the only thing that ever has.” I believe that to be our guiding principle as we embark on this new initiative.

I also believe that students should become specialized in specific areas prior to going fully into “global health,” as they develop in their careers, since they will then add more value later. For example, students should be grounded in the theory of global health in their undergraduate studies and then develop a specialization, such as becoming a statistician, economist, or medical doctor, to make a longer and greater impact in improving global health. As for the business community, we are looking for committed individuals who are specialized in specific areas to bring their knowledge to our organization, as partners in the fight against disease, improving the environment, or helping with humanitarian issues. We are committed to improving health and wellness, increasing access to the best health care, and reducing health disparities.

What is it about your current role that you enjoy the most?

Dr. Marlink: I enjoy building research, learning, and clinical programs, as I have in the HIV arena since the early 1980s. At that time, there were limited resources and funding, but a willingness among universities, non-governmental organizations, hospitals and the pharmaceutical industry to make a difference. Today in my new role, I’d like all of us to have an impact on health and wellness for those in need – to build programs from the ground up while partnering with organizations with the same goal in mind. I know it can be done.

Over my career, when I have a patient here or in a developed country who has been diagnosed with cancer, but is cured or in remission, that puts a huge smile on my face and in my heart. It also impacts you for the rest of your life. Or when I see an infant born without HIV because of the local country programs that are put in place, that also makes me feel so fulfilled, so happy.

I have worked with many talented individuals who have become great friends and partners over my career who have helped create a positive life for under-served populations around the world. We need to remember that progress happens with one person at a time or one program at a time. That’s how you truly improve health around the world.

 

Headshot - 2016

Image SOURCE: Photograph of Inaugural Henry Rutgers Professor of Global Health and Director of the Rutgers Global Health Institute at Rutgers Biomedical and Health Sciences, courtesy of Rutgers University, New Brunswick, New Jersey.

Richard G. Marlink, M.D.
Inaugural Henry Rutgers Professor of Global Health

Director of the Rutgers Global Health Institute

Rutgers Biomedical and Health Sciences

Richard G. Marlink, M.D., a Harvard University professor recognized internationally for research and leadership in the fight against AIDS, was recently appointed as the inaugural Henry Rutgers Professor of Global Health and Director of a new Rutgers Global Health Institute at Rutgers Biomedical and Health Sciences (RBHS). His role is to develop the strategic growth of RBHS by broadening the Rutgers University’s presence in the public health community to improve health and wellness.

Previously, Dr. Marlink was the Bruce A. Beal, Robert L. Beal, and Alexander S. Beal Professor of the Practice of Public Health at Harvard’s T.H. Chan School of Public Health and Executive Director of the Harvard AIDS Initiative.

At the start of the AIDS epidemic, Dr. Marlink was instrumental in setting up the first, hospital-based HIV/AIDS clinic in Boston, Massachusetts, and studied the impact of the HIV virus in west and central Africa. After helping to start the Botswana-Harvard Partnership in 1996, he founded the Kitso AIDS Training Program, which would become Botswana’s national AIDS training program. Kitso means knowledge in the local Setswana language.

Dr. Marlink was the principal investigator for the Tshepo Study, the first large-scale antiretroviral treatment study in Botswana, in addition to conducting other clinical and epidemiological studies in the region. Also in Botswana, he was the country director for Harvard’s contribution to the joint Botswana and United States governments’ HIV/AIDS and TB training, monitoring and evaluation PEPFAR effort.

In the mid-1980s in Senegal, Dr. Marlink was part of the team of Senegalese, French and American researchers who discovered and then studied the second type of human AIDS virus, HIV-2. Since then, he has been involved in multiple HIV/AIDS care, treatment and prevention programs in many African countries, including in Botswana, Côte d’Ivoire (Ivory Coast), Democratic Republic of the Congo, Kenya, Lesotho, Malawi, Mozambique, Rwanda, Senegal, South Africa, Swaziland, Tanzania, Uganda, Zambia and Zimbabwe. He has also organized initiatives to enhance HIV/AIDS care in Brazil, Puerto Rico and Thailand.

Dr. Marlink has served as the scientific director, the vice president for implementation and the senior adviser for medical and scientific affairs at the Elizabeth Glaser Pediatric AIDS Foundation, where he was principal investigator of Project HEART, a five-country CDC/PEPFAR effort in Africa. That project began in 2004 and by 2011 had placed more than 1 million people living with HIV into care clinics. More than 565,000 of these people were placed on life-saving antiretroviral treatment.

Since 2000, Dr. Marlink has been the founding member of the board of directors of the African Comprehensive HIV/AIDS Partnerships, a public-partnership among the government of Botswana and the Bill and Melinda Gates and Merck Foundations to provide ongoing support for numerous HIV/AIDS prevention, care and treatment efforts in that country.

He has authored or co-authored more than 130 scientific articles; written a textbook, Global AIDS Crisis: A Reference Handbook; and co-edited the book, AIDS in Africa, 2nd Edition. Additionally, he served as chief editor for two special supplements to the journal AIDS and as executive editor of the seminal 320-author, three-volume textbook, From the Ground Up: A Guide to Building Comprehensive HIV/AIDS Care Programs in Resource Limited Settings.

A trained fellow in hematology/oncology at the Beth Israel Deaconess Medical Center at Harvard Medical School, Dr. Marlink received his medical degree from the University of New Mexico and his bachelor’s degree from Brown University.

 

Editor’s note:

We would like to thank Marilyn DiGiaccobe, head of Partnerships and Strategic Initiatives, at the Rutgers Global Health Institute, for the help and support she provided during this interview.

 

REFERENCE/SOURCE

Rutgers Biomedical and Health Sciences (http://rbhs.rutgers.edu/)

Other related articles

Retrieved from https://aids.harvard.edu/ 

Retrieved from http://b.3cdn.net/glaser/515eaa8068b5e71d44_mlbrof7xw.pdf 

Other related articles were published in this Open Access Online Scientific Journal include the following: 

2016

CRISPR/Cas9 and HIV1 

https://pharmaceuticalintelligence.com/2016/04/16/crisprcas9-and-hiv1/

Concerns About Viruses

https://pharmaceuticalintelligence.com/2016/01/29/concerns-about-viruses/

CD-4 Therapy for Solid Tumors

https://pharmaceuticalintelligence.com/2016/05/02/cd-4-therapy-for-solid-tumors/

Novel Discoveries in Molecular Biology and Biomedical Science

https://pharmaceuticalintelligence.com/2016/05/30/novel-discoveries-in-molecular-biology-and-biomedical-science/

Scientists eliminate HIV1 DNA from the genome and prevent reinfection

https://pharmaceuticalintelligence.com/2016/03/23/scientists-eliminate-hiv1-dna-from-the-genome-and-prevent-reinfection/

Double Downside of HIV CRISPR therapy

https://pharmaceuticalintelligence.com/2016/04/09/double-downside-of-hiv-crispr-therapy/

2015

Where Infection meets with Cancer: Kaposi’s sarcoma (KS) is the most common cancer in HIV-1-infected persons and is caused by one of only 7 human cancer viruses, i.e., human herpesvirus 8 (HHV-8)

https://pharmaceuticalintelligence.com/2015/10/20/where-infection-meets-with-cancer-kaposis-sarcoma-ks-is-the-most-common-cancer-in-hiv-1-infected-persons-and-is-caused-by-one-of-only-7-human-cancer-viruses-i-e-human-herpesvirus-8-hhv/

Antibody shows promise as treatment for HIV

https://pharmaceuticalintelligence.com/2015/04/09/antibody-shows-promise-as-treatment-for-hiv/

2014

AIDS: Origin of HIV pandemic ‘was 1920s Kinshasa’

https://pharmaceuticalintelligence.com/2014/10/10/aids-origin-of-hiv-pandemic-was-1920s-kinshasa/

2013

Scientists discover how AIDS virus enters key immune cells

https://pharmaceuticalintelligence.com/2013/12/31/scientists-discover-how-aids-virus-enters-key-immune-cells/

Heroes in Medical Research: Dr. Robert Ting, Ph.D. and Retrovirus in AIDS and Cancer

https://pharmaceuticalintelligence.com/2013/04/17/heroes-in-medical-research-dr-robert-ting-ph-d-and-retrovirus-in-aids-and-cancer/

2012

Nanotechnology and HIV/AIDS treatment

https://pharmaceuticalintelligence.com/2012/12/25/nanotechnology-and-hivaids-treatment/

HIV vaccine: Caltech puts us One step further

https://pharmaceuticalintelligence.com/2012/08/31/hiv-vaccine-caltech-puts-us-one-step-further/

Bone Marrow Transplant Eliminates Signs of HIV Infection

https://pharmaceuticalintelligence.com/2012/07/29/bone-marrow-transplant-eliminates-signs-of-hiv-infection/

Getting Better: Documentary Videos on Medical Progress — in Surgery, Leukemia, and HIV/AIDS

https://pharmaceuticalintelligence.com/2012/08/23/getting-better-documentary-videos-on-medical-progress-in-surgery-leukemia-and-hivaids/

Read Full Post »


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Scientists think excessive population growth is a cause of scarcity and environmental degradation. A male pill could reduce the number of unintended pregnancies, which accounts for 40 percent of all pregnancies worldwide.

 

But, big drug companies long ago dropped out of the search for a male contraceptive pill which is able to chemically intercept millions of sperm before they reach a woman’s egg. Right now the chemical burden for contraception relies solely on the female. There’s not much activity in the male contraception field because an effective solution is available on the female side.

 

Presently, male contraception means a condom or a vasectomy. But researchers from Center for Drug Discovery at Baylor College of Medicine, USA are renewing the search for a better option—an easy-to-take pill that’s safe, fast-acting, and reversible.

 

The scientists began with lists of genes active in the testes for sperm production and motility and then created knockout mice that lack those genes. Using the gene-editing technology called CRISPR, in collaboration with Japanese scientists, they have so far made more than 75 of these “knockout” mice.

 

They allowed these mice to mate with normal (wild type) female mice, and if their female partners don’t get pregnant after three to six months, it means the gene might be a target for a contraceptive. Out of 2300 genes that are particularly active in the testes of mice, the researchers have identified 30 genes whose deletion makes the male infertile. Next the scientists are planning a novel screening approach to test whether any of about two billion chemicals can disable these genes in a test tube. Promising chemicals could then be fed to male mice to see if they cause infertility.

 

Female birth control pills use hormones to inhibit a woman’s ovaries from releasing eggs. But hormones have side effects like weight gain, mood changes, and headaches. A trial of one male contraceptive hormone was stopped early in 2011 after one participant committed suicide and others reported depression. Moreover, some drug candidates have made animals permanently sterile which is not the goal of the research. The challenge is to prevent sperm being made without permanently sterilizing the individual.

 

As a better way to test drugs, Scientists at University of Georgia, USA are investigating yet another high-tech approach. They are turning human skin cells into stem cells that look and act like the spermatogonial cells in the testes. Testing drugs on such cells might provide more accurate leads than tests on mice.

 

The male pill would also have to start working quickly, a lot sooner than the female pill, which takes about a week to function. Scientists from University of Dundee, U.K. admitted that there are lots of challenges. Because, a women’s ovary usually release one mature egg each month, while a man makes millions of sperm every day. So, the male pill has to be made 100 percent effective and act instantaneously.

 

References:

 

https://www.technologyreview.com/s/603676/the-search-for-a-perfect-male-birth-control-pill/

 

https://futurism.com/videos/the-perfect-male-birth-control-pill-is-coming-soon/?utm_source=Digest&utm_campaign=c42fc7b9b6-EMAIL_CAMPAIGN_2017_03_20&utm_medium=email&utm_term=0_03cd0a26cd-c42fc7b9b6-246845533

 

http://www.telegraph.co.uk/women/sex/the-male-pill-is-coming—and-its-going-to-change-everything/

 

http://www.mensfitness.com/women/sex-tips/male-birth-control-pill-making

 

http://health.howstuffworks.com/sexual-health/contraception/male-bc-pill.htm

 

http://europe.newsweek.com/male-contraception-side-effects-study-pill-injection-518237?rm=eu

 

http://edition.cnn.com/2016/01/07/health/male-birth-control-pill/index.html

 

http://www.nhs.uk/Conditions/contraception-guide/Pages/male-pill.aspx

Read Full Post »


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

During pregnancy, the baby is mostly protected from harmful microorganisms by the amniotic sac, but recent research suggests the baby could be exposed to small quantities of microbes from the placenta, amniotic fluid, umbilical cord blood and fetal membranes. One theory is that any possible prenatal exposure could ‘pre-seed’ the infant microbiome. In other words, to set the right conditions for the ‘main seeding event’ for founding the infant microbiome.

When a mother gives birth vaginally and if she breastfeeds, she passes on colonies of essential microbes to her baby. This continues a chain of maternal heritage that stretches through female ancestry for thousands of generations, if all have been vaginally born and breastfed. This means a child’s microbiome, that is the trillions of microorganisms that live on and in him or her, will resemble the microbiome of his/her mother, the grandmother, the great-grandmother and so on, if all have been vaginally born and breastfed.

As soon as the mother’s waters break, suddenly the baby is exposed to a wave of the mother’s vaginal microbes that wash over the baby in the birth canal. They coat the baby’s skin, and enter the baby’s eyes, ears, nose and some are swallowed to be sent down into the gut. More microbes form of the mother’s gut microbes join the colonization through contact with the mother’s faecal matter. Many more microbes come from every breath, from every touch including skin-to-skin contact with the mother and of course, from breastfeeding.

With formula feeding, the baby won’t receive the 700 species of microbes found in breast milk. Inside breast milk, there are special sugars called human milk oligosaccharides (HMO’s) that are indigestible by the baby. These sugars are designed to feed the mother’s microbes newly arrived in the baby’s gut. By multiplying quickly, the ‘good’ bacteria crowd out any potentially harmful pathogens. These ‘good’ bacteria help train the baby’s naive immune system, teaching it to identify what is to be tolerated and what is pathogen to be attacked. This leads to the optimal training of the infant immune system resulting in a child’s best possible lifelong health.

With C-section birth and formula feeding, the baby is not likely to acquire the full complement of the mother’s vaginal, gut and breast milk microbes. Therefore, the baby’s microbiome is not likely to closely resemble the mother’s microbiome. A baby born by C-section is likely to have a different microbiome from its mother, its grandmother, its great-grandmother and so on. C-section breaks the chain of maternal heritage and this break can never be restored.

The long term effect of an altered microbiome for a child’s lifelong health is still to be proven, but many studies link C-section with a significantly increased risk for developing asthma, Type 1 diabetes, celiac disease and obesity. Scientists might not yet have all the answers, but the picture that is forming is that C-section and formula feeding could be significantly impacting the health of the next generation. Through the transgenerational aspect to birth, it could even be impacting the health of future generations.

References:

https://blogs.scientificamerican.com/guest-blog/shortchanging-a-babys-microbiome/

https://www.ncbi.nlm.nih.gov/pubmed/23926244

https://www.ncbi.nlm.nih.gov/pubmed/26412384

https://www.ncbi.nlm.nih.gov/pubmed/25290507

https://www.ncbi.nlm.nih.gov/pubmed/25974306

https://www.ncbi.nlm.nih.gov/pubmed/24637604

https://www.ncbi.nlm.nih.gov/pubmed/22911969

https://www.ncbi.nlm.nih.gov/pubmed/25650398

https://www.ncbi.nlm.nih.gov/pubmed/27362264

https://www.ncbi.nlm.nih.gov/pubmed/27306663

http://www.mdpi.com/1099-4300/14/11/2036

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464665/

https://www.ncbi.nlm.nih.gov/pubmed/24848255

https://www.ncbi.nlm.nih.gov/pubmed/26412384

https://www.ncbi.nlm.nih.gov/pubmed/28112736

http://ndnr.com/gastrointestinal/the-infant-microbiome-how-environmental-maternal-factors-influence-its-development/

Read Full Post »


genomicsinpersonalizedmedicinecovervolumeone

Content Consultant: Larry H Bernstein, MD, FCAP

Genomics Orientations for Personalized Medicine

Volume One

http://www.amazon.com/dp/B018DHBUO6

electronic Table of Contents

Chapter 1

1.1 Advances in the Understanding of the Human Genome The Initiation and Growth of Molecular Biology and Genomics – Part I

1.2 CRACKING THE CODE OF HUMAN LIFE: Milestones along the Way – Part IIA

1.3 DNA – The Next-Generation Storage Media for Digital Information

1.4 CRACKING THE CODE OF HUMAN LIFE: Recent Advances in Genomic Analysis and Disease – Part IIC

1.5 Advances in Separations Technology for the “OMICs” and Clarification of Therapeutic Targets

1.6 Genomic Analysis: FLUIDIGM Technology in the Life Science and Agricultural Biotechnology

Chapter 2

2.1 2013 Genomics: The Era Beyond the Sequencing of the Human Genome: Francis Collins, Craig Venter, Eric Lander, et al.

2.2 DNA structure and Oligonucleotides

2.3 Genome-Wide Detection of Single-Nucleotide and Copy-Number Variation of a Single Human Cell 

2.4 Genomics and Evolution

2.5 Protein-folding Simulation: Stanford’s Framework for Testing and Predicting Evolutionary Outcomes in Living Organisms – Work by Marcus Feldman

2.6 The Binding of Oligonucleotides in DNA and 3-D Lattice Structures

2.7 Finding the Genetic Links in Common Disease: Caveats of Whole Genome Sequencing Studies

Chapter 3

3.1 Big Data in Genomic Medicine

3.2 CRACKING THE CODE OF HUMAN LIFE: The Birth of Bioinformatics & Computational Genomics – Part IIB 

3.3 Expanding the Genetic Alphabet and linking the Genome to the Metabolome

3.4 Metabolite Identification Combining Genetic and Metabolic Information: Genetic Association Links Unknown Metabolites to Functionally Related Genes

3.5 MIT Scientists on Proteomics: All the Proteins in the Mitochondrial Matrix identified

3.6 Identification of Biomarkers that are Related to the Actin Cytoskeleton

3.7 Genetic basis of Complex Human Diseases: Dan Koboldt’s Advice to Next-Generation Sequencing Neophytes

3.8 MIT Team Researches Regulatory Motifs and Gene Expression of Erythroleukemia (K562) and Liver Carcinoma (HepG2) Cell Lines

Chapter 4

4.1 ENCODE Findings as Consortium

4.2 ENCODE: The Key to Unlocking the Secrets of Complex Genetic Diseases

4.3 Reveals from ENCODE Project will Invite High Synergistic Collaborations to Discover Specific Targets  

4.4 Human Variome Project: encyclopedic catalog of sequence variants indexed to the human genome sequence

4.5 Human Genome Project – 10th Anniversary: Interview with Kevin Davies, PhD – The $1000 Genome

4.6 Quantum Biology And Computational Medicine

4.7 The Underappreciated EpiGenome

4.8 Unraveling Retrograde Signaling Pathways

4.9  “The SILENCE of the Lambs” Introducing The Power of Uncoded RNA

4.10  DNA: One man’s trash is another man’s treasure, but there is no JUNK after all

Chapter 5

5.1 Paradigm Shift in Human Genomics – Predictive Biomarkers and Personalized Medicine – Part 1 

5.2 Computational Genomics Center: New Unification of Computational Technologies at Stanford

5.3 Personalized Medicine: An Institute Profile – Coriell Institute for Medical Research: Part 3

5.4 Cancer Genomics – Leading the Way by Cancer Genomics Program at UC Santa Cruz

5.5 Genome and Genetics: Resources @Stanford, @MIT, @NIH’s NCBCS

5.6 NGS Market: Trends and Development for Genotype-Phenotype Associations Research

5.7 Speeding Up Genome Analysis: MIT Algorithms for Direct Computation on Compressed Genomic Datasets

5.8  Modeling Targeted Therapy

5.9 Transphosphorylation of E-coli Proteins and Kinase Specificity

5.10 Genomics of Bacterial and Archaeal Viruses

Chapter 6

6.1  Directions for Genomics in Personalized Medicine

6.2 Ubiquinin-Proteosome pathway, Autophagy, the Mitochondrion, Proteolysis and Cell Apoptosis: Part III

6.3 Mitochondrial Damage and Repair under Oxidative Stress

6.4 Mitochondria: More than just the “Powerhouse of the Cell”

6.5 Mechanism of Variegation in Immutans

6.6 Impact of Evolutionary Selection on Functional Regions: The imprint of Evolutionary Selection on ENCODE Regulatory Elements is Manifested between Species and within Human Populations

6.7 Cardiac Ca2+ Signaling: Transcriptional Control

6.8 Unraveling Retrograde Signaling Pathways

6.9 Reprogramming Cell Fate

6.10 How Genes Function

6.11 TALENs and ZFNs

6.12 Zebrafish—Susceptible to Cancer

6.13 RNA Virus Genome as Bacterial Chromosome

6.14 Cloning the Vaccinia Virus Genome as a Bacterial Artificial Chromosome 

6.15 Telling NO to Cardiac Risk- DDAH Says NO to ADMA(1); The DDAH/ADMA/NOS Pathway(2)

6.16  Transphosphorylation of E-coli proteins and kinase specificity

6.17 Genomics of Bacterial and Archaeal Viruses

6.18  Diagnosing Diseases & Gene Therapy: Precision Genome Editing and Cost-effective microRNA Profiling

Chapter 7

7.1 Harnessing Personalized Medicine for Cancer Management, Prospects of Prevention and Cure: Opinions of Cancer Scientific Leaders @ http://pharmaceuticalintelligence.com

7.2 Consumer Market for Personal DNA Sequencing: Part 4

7.3 GSK for Personalized Medicine using Cancer Drugs Needs Alacris Systems Biology Model to Determine the In Silico Effect of the Inhibitor in its “Virtual Clinical Trial”

7.4 Drugging the Epigenome

7.5 Nation’s Biobanks: Academic institutions, Research institutes and Hospitals – vary by Collections Size, Types of Specimens and Applications: Regulations are Needed

7.6 Personalized Medicine: Clinical Aspiration of Microarrays

Chapter 8

8.1 Personalized Medicine as Key Area for Future Pharmaceutical Growth

8.2 Inaugural Genomics in Medicine – The Conference Program, 2/11-12/2013, San Francisco, CA

8.3 The Way With Personalized Medicine: Reporters’ Voice at the 8th Annual Personalized Medicine Conference, 11/28-29, 2012, Harvard Medical School, Boston, MA

8.4 Nanotechnology, Personalized Medicine and DNA Sequencing

8.5 Targeted Nucleases

8.6 Transcript Dynamics of Proinflammatory Genes

8.7 Helping Physicians identify Gene-Drug Interactions for Treatment Decisions: New ‘CLIPMERGE’ program – Personalized Medicine @ The Mount Sinai Medical Center

8.8 Intratumor Heterogeneity and Branched Evolution Revealed by Multiregion Sequencing[1]

8.9 Diagnosing Diseases & Gene Therapy: Precision Genome Editing and Cost-effective microRNA Profiling

Chapter 9

9.1 Personal Tale of JL’s Whole Genome Sequencing

9.2 Inspiration From Dr. Maureen Cronin’s Achievements in Applying Genomic Sequencing to Cancer Diagnostics

9.3 Inform Genomics Developing SNP Test to Predict Side Effects, Help MDs Choose among Chemo Regimens

9.4 SNAP: Predict Effect of Non-synonymous Polymorphisms: How Well Genome Interpretation Tools could Translate to the Clinic

9.5  LEADERS in Genome Sequencing of Genetic Mutations for Therapeutic Drug Selection in Cancer Personalized Treatment: Part 2

9.6 The Initiation and Growth of Molecular Biology and Genomics – Part I

9.7 Personalized Medicine-based Cure for Cancer Might Not Be Far Away

9.8 Personalized Medicine: Cancer Cell Biology and Minimally Invasive Surgery (MIS)

 Chapter 10

10.1 Pfizer’s Kidney Cancer Drug Sutent Effectively caused REMISSION to Adult Acute Lymphoblastic Leukemia (ALL)

10.2 Imatinib (Gleevec) May Help Treat Aggressive Lymphoma: Chronic Lymphocytic Leukemia (CLL)

10.3 Winning Over Cancer Progression: New Oncology Drugs to Suppress Passengers Mutations vs. Driver Mutations

10.4 Treatment for Metastatic HER2 Breast Cancer

10.5 Personalized Medicine in NSCLC

10.6 Gene Sequencing – to the Bedside

10.7 DNA Sequencing Technology

10.8 Nobel Laureate Jack Szostak Previews his Plenary Keynote for Drug Discovery Chemistry

Chapter 11

11.1 mRNA Interference with Cancer Expression

11.2 Angiogenic Disease Research Utilizing microRNA Technology: UCSD and Regulus Therapeutics

11.3 Sunitinib brings Adult acute lymphoblastic leukemia (ALL) to Remission – RNA Sequencing – FLT3 Receptor Blockade

11.4 A microRNA Prognostic Marker Identified in Acute Leukemia 

11.5 MIT Team: Microfluidic-based approach – A Vectorless delivery of Functional siRNAs into Cells.

11.6 Targeted Tumor-Penetrating siRNA Nanocomplexes for Credentialing the Ovarian Cancer Oncogene ID4

11.7 When Clinical Application of miRNAs?

11.8 How mobile elements in “Junk” DNA promote cancer. Part 1: Transposon-mediated tumorigenesis,

11.9 Potential Drug Target: Glycolysis Regulation – Oxidative Stress-responsive microRNA-320

11.10  MicroRNA Molecule May Serve as Biomarker

11.11 What about Circular RNAs?

Chapter 12

12.1 The “Cancer Establishments” Examined by James Watson, Co-discoverer of DNA w/Crick, 4/1953

12.2 Otto Warburg, A Giant of Modern Cellular Biology

12.3 Is the Warburg Effect the Cause or the Effect of Cancer: A 21st Century View?

12.4 Hypothesis – Following on James Watson

12.5 AMPK Is a Negative Regulator of the Warburg Effect and Suppresses Tumor Growth In Vivo

12.6 AKT signaling variable effects

12.7 Rewriting the Mathematics of Tumor Growth; Teams Use Math Models to Sort Drivers from Passengers

12.8 Phosphatidyl-5-Inositol signaling by Pin1

Chapter 13

13.1 Nanotech Therapy for Breast Cancer

13.2 BRCA1 a tumour suppressor in breast and ovarian cancer – functions in transcription, ubiquitination and DNA repair

13.3 Exome sequencing of serous endometrial tumors shows recurrent somatic mutations in chromatin-remodeling and ubiquitin ligase complex genes

13.4 Recurrent somatic mutations in chromatin-remodeling and ubiquitin ligase complex genes in serous endometrial tumors

13.5 Prostate Cancer: Androgen-driven “Pathomechanism” in Early onset Forms of the Disease

13.6 In focus: Melanoma Genetics

13.7 Head and Neck Cancer Studies Suggest Alternative Markers More Prognostically Useful than HPV DNA Testing

13.8 Breast Cancer and Mitochondrial Mutations

13.9  Long noncoding RNA network regulates PTEN transcription

Chapter 14

14.1 HBV and HCV-associated Liver Cancer: Important Insights from the Genome

14.2 Nanotechnology and HIV/AIDS treatment

14.3 IRF-1 Deficiency Skews the Differentiation of Dendritic Cells

14.4 Sepsis, Multi-organ Dysfunction Syndrome, and Septic Shock: A Conundrum of Signaling Pathways Cascading Out of Control

14.5  Five Malaria Genomes Sequenced

14.6 Rheumatoid Arthritis Risk

14.7 Approach to Controlling Pathogenic Inflammation in Arthritis

14.8 RNA Virus Genome as Bacterial Chromosome

14.9 Cloning the Vaccinia Virus Genome as a Bacterial Artificial Chromosome

Chapter 15

15.1 Personalized Cardiovascular Genetic Medicine at Partners HealthCare and Harvard Medical School

15.2 Congestive Heart Failure & Personalized Medicine: Two-gene Test predicts response to Beta Blocker Bucindolol

15.3 DDAH Says NO to ADMA(1); The DDAH/ADMA/NOS Pathway(2)

15.4 Peroxisome Proliferator-Activated Receptor (PPAR-gamma) Receptors Activation: PPARγ Transrepression for Angiogenesis in Cardiovascular Disease and PPARγ Transactivation for Treatment of Diabetes

15.5 BARI 2D Trial Outcomes

15.6 Gene Therapy Into Healthy Heart Muscle: Reprogramming Scar Tissue In Damaged Hearts

15.7 Obstructive coronary artery disease diagnosed by RNA levels of 23 genes – CardioDx, a Pioneer in the Field of Cardiovascular Genomic  Diagnostics

15.8 Ca2+ signaling: transcriptional control

15.9 Lp(a) Gene Variant Association

15.9.1 Two Mutations, in the PCSK9 Gene: Eliminates a Protein involved in Controlling LDL Cholesterol

15.9.2. Genomics & Genetics of Cardiovascular Disease Diagnoses: A Literature Survey of AHA’s Circulation Cardiovascular Genetics, 3/2010 – 3/2013

15.9.3 Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

15.9.4 The Implications of a Newly Discovered CYP2J2 Gene Polymorphism Associated with Coronary Vascular Disease in the Uygur Chinese Population

15.9.5  Gene, Meis1, Regulates the Heart’s Ability to Regenerate after Injuries.

15.10 Genetics of Conduction Disease: Atrioventricular (AV) Conduction Disease (block): Gene Mutations – Transcription, Excitability, and Energy Homeostasis

15.11 How Might Sleep Apnea Lead to Serious Health Concerns like Cardiac and Cancers?

Chapter 16

16.1 Can Resolvins Suppress Acute Lung Injury?

16.2 Lipoxin A4 Regulates Natural Killer Cell in Asthma

16.3 Biological Therapeutics for Asthma

16.4 Genomics of Bronchial Epithelial Dysplasia

16.5 Progression in Bronchial Dysplasia

Chapter 17

17.1 Breakthrough Digestive Disorders Research: Conditions Affecting the Gastrointestinal Tract.

17.2 Liver Endoplasmic Reticulum Stress and Hepatosteatosis

17.3 Biomarkers-identified-for-recurrence-in-hbv-related-hcc-patients-post-surgery

17.4  Usp9x: Promising Therapeutic Target for Pancreatic Cancer

17.5 Battle of Steve Jobs and Ralph Steinman with Pancreatic cancer: How We Lost

Chapter 18

18.1 Ubiquitin Pathway Involved in Neurodegenerative Disease

18.2 Genomic Promise for Neurodegenerative Diseases, Dementias, Autism Spectrum, Schizophrenia, and Serious Depression

18.3 Neuroprotective Therapies: Pharmacogenomics vs Psychotropic Drugs and Cholinesterase Inhibitors

18.4 Ustekinumab New Drug Therapy for Cognitive Decline Resulting from Neuroinflammatory Cytokine Signaling and Alzheimer’s Disease

18.5 Cell Transplantation in Brain Repair

18.6 Alzheimer’s Disease Conundrum – Are We Near the End of the Puzzle?

Chapter 19

19.1 Genetics and Male Endocrinology

19.2 Genomic Endocrinology and its Future

19.3 Commentary on Dr. Baker’s post “Junk DNA Codes for Valuable miRNAs: Non-coding DNA Controls Diabetes”

19.4 Therapeutic Targets for Diabetes and Related Metabolic Disorders

19.5 Secondary Hypertension caused by Aldosterone-producing Adenomas caused by Somatic Mutations in ATP1A1 and ATP2B3 (adrenal cortical; medullary or Organ of Zuckerkandl is pheochromocytoma)

19.6 Personal Recombination Map from Individual’s Sperm Cell and its Importance

19.7 Gene Trap Mutagenesis in Reproductive Research

19.8 Pregnancy with a Leptin-Receptor Mutation

19.9 Whole-genome Sequencing in Probing the Meiotic Recombination and Aneuploidy of Single Sperm Cells

19.10 Reproductive Genetic Testing

Chapter 20

20.1 Genomics & Ethics: DNA Fragments are Products of Nature or Patentable Genes?

20.2 Understanding the Role of Personalized Medicine

20.3 Attitudes of Patients about Personalized Medicine

20.4  Genome Sequencing of the Healthy

20.5   Genomics in Medicine – Tomorrow’s Promise

20.6  The Promise of Personalized Medicine

20.7 Ethical Concerns in Personalized Medicine: BRCA1/2 Testing in Minors and Communication of Breast Cancer Risk

 20.8 Genomic Liberty of Ownership, Genome Medicine and Patenting the Human Genome

Chapter 21

Recent Advances in Gene Editing Technology Adds New Therapeutic Potential for the Genomic Era:  Medical Interpretation of the Genomics Frontier – CRISPR – Cas9

Introduction

21.1 Introducing CRISPR/Cas9 Gene Editing Technology – Works by Jennifer A. Doudna

21.1.1 Ribozymes and RNA Machines – Work of Jennifer A. Doudna

21.1.2 Evaluate your Cas9 gene editing vectors: CRISPR/Cas Mediated Genome Engineering – Is your CRISPR gRNA optimized for your cell lines?

21.1.3 2:15 – 2:45, 6/13/2014, Jennifer Doudna “The biology of CRISPRs: from genome defense to genetic engineering”

21.1.4  Prediction of the Winner RNA Technology, the FRONTIER of SCIENCE on RNA Biology, Cancer and Therapeutics  & The Start Up Landscape in BostonGene Editing – New Technology The Missing link for Gene Therapy?

21.2 CRISPR in Other Labs

21.2.1 CRISPR @MIT – Genome Surgery

21.2.2 The CRISPR-Cas9 System: A Powerful Tool for Genome Engineering and Regulation

Yongmin Yan and Department of Gastroenterology, Hepatology & Nutrition, University of Texas M.D. Anderson Cancer, Houston, USADaoyan Wei*

21.2.3 New Frontiers in Gene Editing: Transitioning From the Lab to the Clinic, February 19-20, 2015 | The InterContinental San Francisco | San Francisco, CA

21.2.4 Gene Therapy and the Genetic Study of Disease: @Berkeley and @UCSF – New DNA-editing technology spawns bold UC initiative as Crispr Goes Global

21.2.5 CRISPR & MAGE @ George Church’s Lab @ Harvard

21.3 Patents Awarded and Pending for CRISPR

21.3.1 Litigation on the Way: Broad Institute Gets Patent on Revolutionary Gene-Editing Method

21.3.2 The Patents for CRISPR, the DNA editing technology as the Biggest Biotech Discovery of the Century

2.4 CRISPR/Cas9 Applications

21.4.1  Inactivation of the human papillomavirus E6 or E7 gene in cervical carcinoma cells using a bacterial CRISPR/Cas 

21.4.2 CRISPR: Applications for Autoimmune Diseases @UCSF

21.4.3 In vivo validated mRNAs

21.4.6 Level of Comfort with Making Changes to the DNA of an Organism

21.4.7 Who will be the the First to IPO: Novartis bought in to Intellia (UC, Berkeley) as well as Caribou (UC, Berkeley) vs Editas (MIT)??

21.4.8 CRISPR/Cas9 Finds Its Way As an Important Tool For Drug Discovery & Development

Summary

Read Full Post »

Older Posts »