Target e*CRF Used in Arthritis & Rheumatism Publication in Polyarticular Juvenile Idiopathic Arthritis

 

 

As part of Target Health’s commitment to academic research, we are pleased to announce that an article entitled “Trial of Early Aggressive Therapy in Polyarticular Juvenile Idiopathic Arthritis” has been published in the December 19, 2011 online edition of Arthritis & Rheumatism. The authors were kind enough to “thank Target Health Inc. for providing and partially subsidizing the electronic data capture system and electronic data base.”

 

This study, started in 2007, was performed to determine if aggressive treatment initiated early in the course of rheumatoid factor positive or negative polyarticular juvenile idiopathic arthritis (poly-JIA) can induce clinical inactive disease (CID) within 6 months. The study was conducted in 85 children aged 2 to 16 years with poly-JIA of less than 12 months duration. In Arm 1, patients received either methotrexate, etanercept, and prednisolone, or methotrexate (same dose as Arm 1), or etanercept placebo, and prednisolone placebo (Arm 2).

 

Results showed that by 6 months, 17 of 42 (40%) of patients in Arm 1 and 10 of 43 (23%) in Arm 2 had achieved CID (p = 0.088), and after 12 months, 9 patients in Arm 1 and 3 in Arm 2 achieved clinical remission on medication (p = 0.0534).

 

According to Dr. Carol Wallace and her passionately dedicated team, although this study did not meet its primary endpoint, early aggressive therapy in this cohort of children with recent onset polyarticular JIA resulted in substantial proportions of patients in both arms achieving CID by 6 months and clinical remission on medication within 12 months of treatment.

 

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at www.targethealth.com

Hayflick Limit

 

 

Human chromosomes (grey) capped by telomeres (white)

 

 

 

The Hayflick limit (or Hayflick Phenomenon) is the number of times a normal cell population will divide before it stops, presumably because the telomeres reach a critical length. The Hayflick limit was discovered by Leonard Hayflick in 1961, at the Wistar Institute, Philadelphia, when Hayflick demonstrated that a population of normal human fetal 1) ___ in a cell culture divide between 40 and 60 times. It then enters a senescence phase (refuting the contention by Alexis Carrel that normal cells are immortal). Each mitosis shortens the telomeres on the DNA of the cell. Telomere shortening in 2) ___ eventually makes cell division impossible, and it correlateswith aging. This mechanism appears to prevent genomic instability and the development of cancer.

 

Prior to Hayflick’s discovery, it was believed that vertebrate cells had an unlimited potential to replicate. Alexis Carrel, a Nobel prize-winning surgeon, had stated “that all cells explanted in culture are immortal, and that the lack of continuous cell replication was due to ignorance on how best to cultivate the cells”. He supported this hypothesis by claiming to have cultivated fibroblasts from chick hearts, and to have kept the 3) ___ growing for 34 years. This indicated that cells of vertebrates could continue to divide indefinitely in a culture. However, other scientists were unable to reproduce Carrel’s result. In fact, Carrel’s result was due to an error in his experimental procedure: chick embryonic 4) ___ cells were added to the culture daily. This allowed for the cultivation of new fresh cells in the culture, and not simply the infinite reproduction of the original cells present in the culture. Dr. Hayflick first became suspicious of Carrel’s theory while working in a lab at the Wistar Institute. Hayflick was preparing normal human cells to be exposed to extracts of cancer cells when he noticed the normal cells had stopped proliferating. At first he thought that he had made a technical error in preparing the experiment, but later he began to think that the cell division processes had a counting mechanism. Working with Paul Morehead, he designed an experiment that showed the truth about normal cell 5) ___.

 

The experiment proceeded as follows. Hayflick and Morehead mixed equal numbers of normal human male fibroblasts that had divided many times (cells at the 40th population doubling) with female fibroblasts that had divided only a few times (cells at the 10th population doubling). Unmixed cell populations were kept as 6) ___. When the male “control” culture stopped dividing, the mixed culture was examined and only female cells were found. This showed that the old cells “remembered” they were old, even when surrounded by young cells, and that technical errors or contaminating viruses were unlikely explanations as to why only the male cell component had died.The cells had stopped dividing and become senescent based purely upon how many times the cell had 7) ___. These results disproved the immortality theory of Carrel and established the Hayflick Limit as accredited biological theory which, unlike the experiment of Carrel, has been reproduced by other scientists. Hayflick describes three phases in the 8) ___ of a cell. At the start of his experiment he named the primary culture “phase one.” Phase two is defined as the period when cells are proliferating — Hayflick called it the time of “luxuriant growth”. After months of doubling the cells eventually reach phase three, a phenomenon of senescence — cell growth diminishes and then stops altogether.

 

This limit has been found to correlate with the length of the telomere region at the end of a strand of 9) ___. During the process of DNA replication, small segments of DNA at each end of the DNA strand (telomeres) are unable to be copied and are lost after each time DNA is duplicated.The telomere region of DNA does not code for any protein; it is simply a repeated code on the end region of DNA that is lost. After many divisions, the telomeres become depleted and the cell begins apoptosis, or cell 10) ___. This is a mechanism that prevents replication error that would cause mutations in DNA. Once the telomeres are depleted due to the cell dividing many times, the cell will no longer divide and the Hayflick limit has been reached.

 

This process errs in cancer cells. 11) ___ cells turn on an enzyme called telomerase which is able to restore telomere length. Thus the telomere of cancer cells is never shortened, giving these cells infinite replicative potential.A proposed treatment for cancer is a telomerase inhibitor that would prevent the restoration of the telomere, allowing the cell to 12) ___ like other body cells.On the other hand, telomerase activators might repair or perhaps extend the telomeres, thus extending the Hayflick limit of healthy cells. This might strengthen the telomeres of immune system cells enough to prevent cancerous cells from developing from cells with very short telomeres. Carnosine can increase the Hayflick limit in human fibroblasts, and also appears to reduce the rate of telomere shortening.

 

ANSWERS: 1) cells; 2) humans; 3) culture; 4) stem; 5) division; 6) controls; 7) divided; 8) life; 9) DNA; 10) death; 11) Cancer; 12) die

Leonard Hayflick 1928 to Present

 

 

Leonard Hayflick Ph.D., is Professor of Anatomy at UCSF. He is a past president of the Gerontological Society of America and was a founding member of the council of the National Institute on Aging (NIA). Hyflick has studied the aging process for more than 30 years and is known for discovering that human cells divide for a limited number of times in vitro (refuting the contention by Alexis Carrel that normal body cells are immortal). This is known as the Hayflick limit.

 

Leonard Hayflick was born May 20, 1928 in Philadelphia, Pennsylvania. He received his Ph.D. at the University of Pennsylvania in 1956. After receiving a post-doctoral Fellowship for study at the University of Texas, Galveston, under the tutelage of the renowned cell culturist Prof. Charles M. Pomerat, he returned to Philadelphia, where he spent ten years as an Associate Member of the Wistar Institute and two years as an Assistant Professor of Research Medicine at the University of Pennsylvania. In 1968 Hayflick was appointed Professor of Medical Microbiology at the Stanford University School of Medicine, Stanford, California. In 1982 he moved to the University of Florida, Gainesville, where he became Director of the Center for Gerontological Studies and Professor of Zoology in the College of Liberal Arts and Sciences and Professor of Microbiology and Immunology in the College of Medicine.

 

In 1988 Hayflick joined the faculty of the University of California, San Francisco where he is presently Professor of Anatomy. Hayflick is a member of numerous national and international scientific and public boards of directors and committees. He is now, or has been, on the Editorial Boards of more than ten professional journals. Hayflick was Editor-in-Chief of the international journal “Experimental Gerontology” for 13 years.

 

Hayflick is known for his research in cell biology, virus vaccine development, and mycoplasmology. In 1962 he discovered that, contrary to the belief prevalent at the turn of the century, cultured normal human and animal cells have a limited capacity for replication. This discovery, known as the Hayflick limit, overturned a dogma that existed since Alexis Carrel’s work early in this century that claimed that normal cells would proliferate continuously in culture. Hayflick’s results focused attention on the finite cellular life-span was the fundamental location of age changes and that immortality was a key feature of tumor cells. Hayflick demonstrated for the first time that mortal (normal) and immortal (malignant) mammalian cells existed.

 

Hayflick developed the first normal human diploid cell strains for studies on human aging and for research use throughout the world. Before his seminal research all cultured cell lines were immortal and aneuploid. One such cell strain, developed by Hayflick and his colleague Paul Moorehead at the Wistar Institute, called WI-38, was the most widely used and highly characterized normal human cell population in the world. Hayflick produced the first oral polio vaccine made on a continuously propagated cell strain. WI-38 is now used for the production of all of the Rubella Virus vaccine used in the Western Hemisphere. WI-38, or new diploid cell strains, is used today for the manufacture of most human virus vaccines produced throughout the world including those for poliomyelitis, rubella, rubeola, varicella, mumps, rabies, adenoviruses and hepatitis A. Over one billion vaccinees have received vaccines produced on WI-38 or foreign version of Hayflick’s original WI-38.

 

Hayflick is also known for his discovery of the cause of primary atypical pneumonia (“walking pneumonia”) in humans. The etiological agent was first thought to be a virus, but Hayflick showed that it was, in fact, a mycoplasma, a member of the smallest free-living class of microorganisms. The etiological agent was named by him as Mycoplasma pneumoniae, and was first grown by Hayflick on a medium he developed and that bears his name. It is now used worldwide for mycoplasma isolation and research.

 

The inverted microscope that Hayflick modified for use in of his tissue culture and mycoplasma work and on which all other such microscopes have been modeled has been acquired by the Smithsonian National Museum of American History.

High Animal Fat Diet Increases Gestational Diabetes Risk

 

 

Gestational diabetes is a form of diabetes seen during pregnancy. Gestational diabetes increases the risk for certain pregnancy complications and health problems in the newborn. According to an article published online in the American Journal of Clinical Nutrition (18 January 2012), women who consumed a diet high in animal fat and cholesterol before pregnancy were at higher risk for gestational diabetes than women whose diets were lower in animal fat and cholesterol. In contrast, women whose diets were high in total fat or other kinds of fats-but not in animal fat or cholesterol– did not have an increased risk. Moreover, the increased risk for gestational diabetes seen with animal fat and cholesterol appeared to be independent of other, dietary and non-dietary, risk factors for gestational diabetes. For example, exercise is known to reduce the risk of gestational diabetes. Among women who exercised, however, those who consumed higher amounts of animal fat and cholesterol had a higher risk than those whose diets were lower in these types of fat.

 

According to the authors, the findings indicate that women who reduce the proportion of animal fat and cholesterol in their diets before pregnancy may lower their risk for gestational diabetes during pregnancy, and that changing the source of 5% of dietary calories from animal fat to plant-derived sources could decrease a woman’s risk for gestational diabetes by 7%.

 

The U.S. Department of Agriculture website, ChooseMyPlate.gov, contains information on healthy eating for children and adults, as well as health and nutrition information for pregnant and breast feeding women.

 

The study utilized information from more than 13,000 women participating in the Nurses’ Health Study II. The women were 22 to 45 years old when they enrolled in the study. Every two years they responded to questions on their general health, pregnancy status, and lifestyle habits, such as consuming alcohol or smoking. In addition, every four years they completed a comprehensive survey about the kinds of food and drink they consumed. About 6% of the participants reported having been diagnosed with gestational diabetes. The study then calculated the amount of animal fat in participants’ diets as a % of age of total calories and divided participants into five groups, or quintiles, based on those % of ages. Then the risk for developing gestational diabetes was compared for each group. Women in the highest quintile of intake had almost double the risk for gestational diabetes compared to women in the lowest quintile. Results also showed that women in the highest quintile for cholesterol consumption were 45% more likely to develop gestational diabetes than were women in the lowest quintile.

Caffeine Consumption Linked to Estrogen Changes with Moderate Caffeine Intake Associated with Higher Level for Asians, Lower for Whites

 

 

A total of 89% of U.S. women from 18-34 years of age consume the caffeine equivalent of 1.5 to two cups of coffee a day.

 

According to an article published online in the American Journal of Clinical Nutrition (11 January 2012), Asian women who consumed an average of 200 milligrams or more of caffeine a day — the equivalent of roughly two cups of coffee — had elevated estrogen levels when compared to women who consumed less, according to a study of reproductive age women. However, white women who consumed 200 milligrams or more of caffeine a day had slightly lower estrogen levels than women who consumed less. Black women who consumed 200 milligrams or more of caffeine a day were found to have elevated estrogen levels, but this result was not statistically significant.

 

Total caffeine intake was calculated from any of the following sources: coffee, black tea, green tea, and caffeinated soda. As a result, the findings differed slightly when the source of caffeine was considered singly. Consuming 200 milligrams or more of caffeine from coffee mirrored the findings for overall caffeine consumption, with Asians having elevated estrogen levels, whites having lower estrogen levels, and the results for blacks not statistically significant. However, consumption of more than one cup each day of caffeinated soda or green tea was associated with a higher estrogen level in Asians, whites, and blacks.

 

While studies conducted in animals had suggested that caffeine might interfere with ovulation, the changes in estrogen levels among the women who took part in the study did not appear to affect ovulation.

 

According to Enrique Schisterman, Ph.D., of the Division of Epidemiology, Statistics and Prevention Research at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH institute where some of the research was conducted, the results indicate that caffeine consumption among women of child-bearing age influences estrogen levels, but short term, these variations in estrogen levels among different groups do not appear to have any pronounced effects. Dr. Schisterman added that since we know that variations in estrogen level are associated with such disorders as endometriosis, osteoporosis, and endometrial, breast, and ovarian cancers and because long term caffeine consumption has the potential to influence estrogen levels over a long period of time, it makes sense to take caffeine consumption into account when designing studies to understand these disorders.

 

More than 250 women from 18 to 44 years old participated in the study between 2005 and 2007. On average, they consumed 90 milligrams of caffeine a day, approximately equivalent to one cup of caffeinated coffee. Most of the participants in the study reported to the study clinic one to three times a week for two menstrual cycles. Their visits were scheduled to correspond with specific stages of the menstrual cycle. At the visits, the women reported what they had eaten in the last 24 hours and answered questions about their exercise, sleep, smoking and other aspects of their lifestyle and reproductive hormone levels were measured in blood. The study authors noted that collection of these details during multiple time points across two menstrual cycles produced more precise information about the link between caffeine and hormones than was possible in earlier studies. The authors also noted that the study participants were more racially diverse than those who took part in previous studies.

Elevated Risk Factors Linked to Major Cardiovascular Disease Events

 

 

According to an article published in the New England Journal of Medicine (2012;366:321-329), an NIH-supported project analyzed data from 18 population-based studies, involving over 250,000 people. In one of the largest-ever analyses of lifetime risks for cardiovascular disease (CVD), it was found that middle-aged adults who have one or more elevated traditional risk factors for CVD, such as high blood pressure, have a substantially greater chance of having a major CVD event, such as heart attack or stroke, during their remaining lifetime than people with optimal levels of risk factors. This NIH-supported study used health data from 257,384 people and was the first to look simultaneously at multiple risk factors for CVD across age, gender, race, and birth generation.

 

According to Susan B. Shurin, M.D., acting director of the NIH’s National Heart, Lung, and Blood Institute, the paper adds to the substantial body of evidence that modifiable cardiovascular disease risk factors in healthy men and women heavily influence the likelihood of developing cardiovascular disease later in life, regardless of their backgrounds.

 

As part of the Cardiovascular Lifetime Risk Pooling Project, investigators analyzed 50 years of data from 18 existing cohort, or population-based, studies in the United States. The investigators pooled the data from the 18 cohorts and measured traditional CVD risk factors – including high blood pressure, high cholesterol levels, diabetes, and smoking status – in men and women from both black and white populations at ages 45, 55, 65, and 75 years.

 

Results showed that men who were 55 years old with at least two major risk factors were six times as likely to die from CVD by age 80 as were men with none or one CVD risk factor (29.6% vs. 4.7%). Women with at least two major risk factors were three times as likely to die from CVD as were women with no or one CVD risk factor (20.5% vs. 6.4%).

 

When all CVD events – fatal and non-fatal – were considered, the results were even more striking. Forty-five-year-old men with two or more risk factors had a 49.5% chance of having a major CVD event through age 80, while 45-year-old women had a 30.7% chance. On the other hand, men with optimal risk factor levels only had a 1.4% chance of having a major CVD event, while women had a 4.1% chance of having a major CVD event through age 80.

 

The results from each individual study were consistent with one another and with those of the pooled group, and showed that traditional risk factors predicted a person’s long-term development of CVD more than age. All of the risk factors appeared to carry the same levels of risk as they did 20, 30, or 40 years ago. While black Americans had a higher prevalence of CVD risk factors than white Americans, their lifetime risks were similar when their risk factor profiles were similar.

TARGET HEALTH excels in Regulatory Affairs. Each week we highlight new information in this challenging area.

 

 

FDA Approves Inlyta to Treat Patients with Advanced Renal Cell Carcinoma

 

 

Renal cell carcinoma is a type of kidney cancer that starts in the lining of very small tubes in the kidney.

 

The FDA has approved Inlyta (axitinib; Pfizer) to treat patients with advanced kidney cancer (renal cell carcinoma) who have not responded to another drug for this type of cancer. Inlyta, a pill that patients take twice a day, works by blocking certain proteins called kinases that play a role in tumor growth and cancer progression.

 

This is the seventh drug that has been approved for the treatment of metastatic or advanced kidney cell cancer since 2005. According to FDA, collectively, this unprecedented level of drug development within this time period has significantly altered the treatment paradigm of metastatic kidney cancer, and offers patients multiple treatment options. Recently approved drugs for the treatment of kidney cancer include sorafenib (2005), sunitinib (2006), temsirolimus (2007), everolimus (2009), bevacizumab (2009) and pazopanib (2009).

 

The safety and effectiveness of Inlyta were evaluated in a single randomized, open-label, multi-center clinical study of 723 patients whose disease had progressed on or after treatment with one prior systemic therapy. The study was designed to measure progression-free survival, the time a patient lived without the cancer progressing. Results showed a median progression-free survival of 6.7 months compared to 4.7 months with a standard treatment (sorafenib).

 

The most common side effects observed in greater than 20% of patients in the clinical study were diarrhea, high blood pressure (hypertension), fatigue, decreased appetite, nausea, loss of voice (dysphonia), hand-foot syndrome (palmar-plantar erythrodysesthesia), weight loss, vomiting, weakness (asthenia) and constipation.

 

Patients with high blood pressure should have it well-controlled before taking Inlyta. Some patients who took Inlyta experienced bleeding problems, which in some cases were fatal. Patients with untreated brain tumors or gastrointestinal bleeding should not take Inlyta.

Year of the Dragon

 

Lincoln Center, NYC, Jan 24, 2012, Gala Performance of Nai-Ni Chen Dance Company

 

 

Dragon Dance at Lincoln Center, NYC, on Tuesday 24th January 2012, with Lang Lang the Great Chinese Pianist, Gala Concert Celebration

 

 

Credit:Ramin Talaie for The Wall Street Journal

               Dragon Dancers Herald the Start of Lunar New Year at Roosevelt Park in Manhattan’s Chinatown

 

 

2012 Lunar New Year in Boston, MA, USA

 

 

Former North Koreans, now living in South Korea, release cake snacks in balloons, to go over the border, to celebrate 2012 Year of the Dragon

 

 

New Year’s  Tet Celebration Market Display in Ho Chi Minh City, Vietnam

 

 

2012 Celebrating the New Year in Saigon

 

 

Traditional Decoration for New Year in Japan

 

 

Hong Kong

 

 

Kuala Lumpur, Malasia

 

 

2012 New Year’s Feast in Mongolia

 

 

2012 Traditional New Year Game in Korea

 

 

2012 Year of Dragon Celebration in Mijas, Spain

 

 

2012 New Year Celebration in Tibet

 

 

Korea

 

 

South Korean Soldiers Celebrate the Lunar New Year, bowing with respect to ancestors.

 

 

Singapore

 

 

Hanoi, Vietnam

 

 

Taiwan

 

 

Bangkok, Thailand

 

 

Seoul, Korea

 

 

Manila, Philippines

 

 

Seoul, Korea

 

 

Cambodia

 

 

Chinatown, Lima, Peru

 

 

Singapore

 

 

Cambodia

 

 

Shanghai

 

 

Jakarta

 

 

Beijing

 

 

Central Java

 

 

Jakarta

 

 

Manila, Philippines

 

 

Indonesia

 

 

North Sumatra

 

 

Thailand

 

 

Manila, Philippines

Glen Park Selected as Review Editor of Frontiers in Pharmaceutical Medicine and Outcomes Research

 

 

We are pleased to announce that in addition to  Sr. Director of Clinical Research and Regulatory Affairs at Target Health Inc.,  Dr. Glen Park, has accepted the position and the challenge to serve as Review Editor of Frontiers in Pharmaceutical Medicine and Outcomes Research. Frontiers aims to change the world of academic research publishing to ensure high quality peer-reviewing, equal opportunity to publish and read, drive integration across disciplines, provide a spectrum of services for researchers and research-related organizations, and systematically translate advanced research knowledge to increase public understanding. The Frontiers vision is a comprehensive full-service system for all entities concerned with academic research.

 

The “Frontiers in” journal series operates as open access journals and, therefore, adopts the standard open access business model where authors pay the Article Publishing Fees (APF) to allow anyone to read their article for free (author-pay/reader-free). Frontiers has successfully pioneered its equal-opportunity publishing model in the field of Neuroscience and now aims to offer this model to fields across all of academia. The vision of Frontiers is to build the complete Tree of Academia and create a single platform for integration across fields.

 

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at www.targethealth.com

New Way to Learn About and Potentially Block Traits in Harmful Pathogens

 

Electron micrograph of Chlamydia mutant bacteria inside of a cell. These particular mutant bacteria, colored red, are defective in secreting high levels of virulence proteins, seen here as the accumulating dark granules in between two bacterial membranes. (Credit: Bidong Nguyen, Duke Molecular Genetics and Microbiology)

 

 

 

Researchers at Duke University Medical Center have developed a new way to identify the genes of harmful 1) ___, particularly those that have been difficult to study in the laboratory. This new method uses chemicals to create mutant bacteria, followed by genomic sequencing to identify all mutations. By looking for common genes that were mutated in Chlamydia sharing a particular trait, the investigators were able to rapidly “zero in” on the genes responsible for that 2) ___. The approach is versatile and inexpensive enough that it could be applied to study a range of microorganisms, said Raphael Valdivia, PhD, an associate professor of molecular genetics and microbiology at Duke. “We were able to learn about 3) ___ that allow Chlamydia to flourish in their hosts without the traditional, lengthy process of domesticating the pathogen to accept recombinant DNA,” Valdivia said. “Our approach marries classical microbiology techniques with 21st century genome-4) ___ technologies. If you encounter a new dangerous microorganism and want to determine what genes are important, I think this represents an effective way to learn all we can, as fast as we can.” The work was published on Jan. 9 in the early edition of the Proceedings of the National Academy of Sciences.

 

One of the goals in studying microbial pathogens that harm 5) ___ and animals is to locate and disrupt the genes required for infection. The microbe in this study, Chlamydia, an STD which hides in human cells, and is a type of 6) ___ that must cause disease to be transmitted from one host to another. Chlamydia is the leading STD infection and a risk factor for pelvic inflammatory disease and infertility.

 

Prior to this work, the function of many 7) ___ genes had to be inferred by their similarity to genes from other bacteria. “By isolating mutants that don’t grow well inside cells and identifying the underlying mutations, we can learn a lot about how these genes contribute to disease,” Valdivia said. “These are the activities we’d like to block.” “For us, this significantly accelerates the analysis of Chlamydia and importantly, should be applicable to many other microbes that have been difficult manipulate with recombinant DNA approaches,” he said.

 

Valdivia suggested that even microbes associated with our normal intestinal flora, which are notoriously difficult to manipulate, are now open to exploration so that we can learn how their genes influence human health, including dietary disorders and inflammatory bowel 8) ___.

 

Valdivia also said that the new technique could help to create Chlamydia 9) ___ that have a combination of mutations that affect the pathogen’s virulence. “That way we can cripple some aspects of the bacterium’s ability to thrive intact in a host, while still allowing the bacterium to replicate enough to prime the immune 10) ___ against it.”

 

ANSWERS: 1) microbes; 2) trait; 3) genes; 4) sequencing; 5) humans; 6) bacteria; 7) Chlamydia; 8) disease; 9) vaccines; 10) system

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