A Genetics Nurse helps patients with or at risk for diseases related to their genetics, diseases like cancer, heart disease, diabetes, and Alzheimers. These nurses perform risk assessments and analyze the data found. A career in Genetics Nursing can be very rewarding, youll help patients and families better prepare themselves for the potentially harmful diseases that run in their family.

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Genetics Nurse | Discover Nursing

The Department of Genetics and Human Genetics offers courses leading to the Master of Science and Doctor of Philosophy degrees . The program is associated with the Departments of Pediatrics and Biology so that students will not only learn to work creatively in their own field of special interest but will also be able to relate their findings to progress made in related disciplines.

The graduate programs in Genetics & Human Genetics are designed to confer the training standards that will develop students for degrees of Doctorate of Philosophy Masters, and M.D./Ph.D. degree(s). The graduate program is an interdepartmental entity built on a diverse platform.

The program is associated with the department of Pediatrics and department of Biology where students work creatively in their field of special interest but and be able to relate application and relevance to related clinical and science disciplines.

The degree programs are designed to provide a curricular foundation in human genetics for all enrolled students during their first year.Following this, guided by their academic adviser, students elect to pursue their area of interest in genetics . This is accomplished through a combination of elective courses offered in the Department and other departments of the University, as well as in the Washington Area Consortium of Universities. The Masters thesis and Doctoral dissertation research interests likewise can reflect a broad range of interests, provided a suitable research mentor is identified in the graduate faculty.

This training program design takes into account the fact that genetics is increasingly relevant within the framework of multiple biomedical research and scholarly pursuits. The program design also is intended to foster the important principle of collaborative research and scholarship among biomedical disiplines.

The graduate programs are research-oriented curriculum's in the study of genetic mechanisms related to the transition from normal to disease states and intended to prepare graduates to participate in laboratory research.

To be accepted into the Graduate Program in Genetics and Human Genetics, students must have a Bachelors degree from an accredited institution and a GPA of at least 3.0 or B equivalent. In addition, students must meet the University requirement(s) to take the Graduate Record Examination (and the TOEFL if applicable).

Students with a bachelor degree may enter the graduate program at the Masters level or directly into the Ph.D. program. Eligibility to be considered for direct admission as a Ph.D. student requires a cumulative GPA greater than 3.2 and prior research and/or training experience in during undergraduate school or during a previous Masters degree

Applicants are required to submit these items for consideration of acceptance and review of potential for success:

Students wishing to enter the master's program should have a baccalaureate degree and a cumulative GPA average of B or the equivalent. They also should have completed undergraduate courses in modern biology, chemistry through organic chemistry, general biochemistry, mathematics through calculus, and general genetics, or equivalent courses. These prerequisites apply regardless of specialization selected within the master's program.

Students with less than a B average or who have not completed all of the required undergraduate courses may be admitted conditionally if they have very high Graduate Record Examination scores and/or excellent recommendations.

Students may matriculate into the doctoral program, having completed a suitable Masters degree, provided they present evidence of previous research experience supported by excellent letters of recommendation, and grades above 3.2 average.

Students who do not meet these general criteria may be considered for the master's program as indicated above.

The degree programs are designed to provide a curricular foundation in human genetics during their first and second year. Following years students elect to pursue elective courses in their area of interest.

Classes for degree credits are gained through a combination of elective courses offered in the Department, other departments within the University, and from courses offered through the Washington Area Consortium of Universities.

To confer the degree of Masters in Science requires;

To confer the degree of Doctor of Philosophy requires;

The College of Medicine and the Graduate School jointly offer an integrated program that leads to both the M.D. and Ph.D. degrees without compromise in the customary substance of each of these degrees individually. Additionally, the curricular emphasis develops in the trainee the unique professional role perspective of the clinician/scientist/scholar. It also develops a particular appreciation for the urgent and unsolved health problems that are present in the population served by the Howard University Hospital and its affiliated clinical programs.

Application Process

Graduate departments that currently invite applications for Ph.D. study in this program are: Anatomy, Biochemistry and Molecular Biology, Biology, Chemistry, Communication Sciences and Disorders, Genetics and Human Genetics, Microbiology, Pharmacology, Physiology and Biophysics.

The steps in the application process are as follows:

The application for the M.D./Ph.D. program shou ld be returned to:

Kareem Washington, Ph.D.Director M.D./Ph.D. ProgramHoward University College of Medicine520 W Street, NWWashington, DC 20059email:kareem.washington @howard.edu

A student, with the advice of the director of graduate studies, may file for admission to candidacy.

Students in the Ph.D. program are required to spend at least three semesters in full-time residence, two of which must be consecutive.

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Genetics and Human Genetics | Graduate School

Thank you for visiting Goodstartgenetics.com. Good Start has been acquired by Invitae.

As of June 25, 2018, carrier screening is available to order through Invitae. If youre looking to access an order status placed prior to June 25, 2018, please login to your Gateway account.

Invitae Preimplantation Genetic Testing (PGT) ordering and order status is still available through your Gateway account.

Please visit Invitae to learn more about reproductive health testing for your patients.

If your doctor has ordered carrier screening for you prior to June 25, 2018, you may access your results and payment options by visiting the PersonalVu patient portal. For new patients, please log in to the Invitae patient portal to view your results and order status.

If your doctor has ordered preimplantation genetic testing for you, please log into the PersonalVu patient portal to watch our educational video, sign your informed consent and pay your bill.

Please visit Invitae to learn more about our reproductive health testing options.

For any additional questions, please contact Invitae.

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Good Start Genetics

Diagnostic genetics services at Boston Medical Center provide expertise in the diagnosis and evaluation of genetic and developmental disorders for patients, including:

Medical geneticist Jodi Hoffman, MD and the genetics teammanagement services for adults who have inherited disorders, genetic conditions, or birth defects. Patients seen in this clinic often have connective tissue disorders (Marfan syndrome and Ehlers Danlos syndrome, etc) as well as neurofibromatosis types 1 and 2, tuberous sclerosis, Down syndrome, rare cancer syndromes, and others. Consultations are provided in the Yawkey Ambulatory Care Clinic, 6th floor. NOTE: This is the same location as pediatric genetics.

For an appointment call 617.414.4841 or fax 617.414.5741

For more information, please call: 617.638.4317

Center of Excellence in Sickle Cell DiseaseHemoglobin Diagnostic Reference LaboratoryFor more information, please call: 617.414.1024.Medical Director: David Chui, MD

Jodi Abbott, MDRobert Blatman, MDPhilip Connors, MS, CGCAviva Lee-Parritz, MDGlenn Markenson, MDLillian Sosa, MS, CGCChristina Yarrington, MD

For an appointment, call 617.414.2000Antenatal Testing Unit: Yawkey5th Floor

Our certified genetic counselors provide consultation and testing for cancer predisposition syndromes for people who have a strong personal or family history of certain types of cancer. Identifying a genetic cause for cancer in a family allows for increased surveillance and earlier detection for at risk family members. The team works with testing companies and insurance to obtain coverage for this testing. Consultations are provided in the Moakley Building, 3rd floor, at 830 Harrison Ave.

For an appointment call: 617.638.6428Referrals can be faxed to: 617.414.1558

Medical geneticist Jodi Hoffman, MD and the genetics teamprovide diagnostic and management services for children who are likely to have inherited disorders, genetic syndromes, or birth defects. Children with unusual physical characteristics, developmental days, autism, or atypical growth are often referred for a genetics evaluation to determine if a genetic condition could explain the constellation of features. A diagnosis may provide information important for future health management as well as connections with support groups, research opportunities, and other families who have children with related conditions. Consultations are provided in the Yawkey Ambulatory Care Clinic, 6th floor.

For an appointment call 617.414.4841 orfax 617.414.5741More information

Certified genetic counselors Philip Connorsand Lillian Sosa provide consultation and counseling in the antenatal unit at Boston Medical Center to women who are pregnant or considering a pregnancy. Reasons for visits include advanced maternal age, abnormal nuchal translucency or maternal serum screening, medication exposures, carrier status, and family history. Clinic is held in Boston Medical Centers Antental Center, Yawkey 5th Floor.

For an appointment call 617.414.2000 orfax 617.414.7657More information

For more information:

Raveen Basran, D.Phil. Director of Diagnostic Molecular Genetics ([emailprotected]: 617.414.5329)Tom Maher, MS, Laboratory Manager of Diagnostic Molecular Genetics ([emailprotected]: 617.414.5312)Dan Remick, MD Medical Director, Diagnostic Molecular GeneticsDownload Diagnostic Genetics Consent Form

Michael OBrien, MD Chief Anatomic PathologyCarl O'Hara, MD - Chief of Laboratory MedicineShi Yang, MD, Scientific DirectorDownload Tissue Based DMP Requisition Form

Nancy Miller, MD, Medical Director Microbiology ([emailprotected])Chris Andry, PhD, Administrative Director and Vice Chair for Pathology Operations and Management ([emailprotected])Neil ONeill, Senior Manager for Laboratory Medicine Operations([emailprotected]: 617.414.4737)

All molecular genetics testing at BMC should be processed via the BMC Laboratory. BMC uses Quest Diagnostics as a reference laboratory and performs some testing in house. Quest Diagnostics' highly trained geneticists and genetic counselors are available at 1.866.GENE.INFO, (1.866.436.3463)

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Genetic Services | Boston Medical Center

Seattle Genetics (NASDAQ:SGEN) saw salesof its only approved drug Adcetris jump substantially in the second quarter, thanks to the Food and Drug Administration approval for the frontline treatment of stage III and IV Hodgkin lymphoma, which was granted in the first quarter.

Metric

Q2 2018

Q2 2017

Year-Over-Year Change

Revenue

$170.2 million

$108.2 million

57%

Income from operations

($30.3 million)

($59.3 million)

N/A

Earnings per share

$0.47

($0.39)

N/A

Data source: Seattle Genetics.

Image source: Getty Images.

"This is the highest sequential quarter-to-quarter growth rate since the product was launched," said Darren Cline, Seattle Genetics' executive vice president of commercial, which shows how big the approval for frontline Hodgkin lymphoma was for the company.

Nevertheless, CEO Clay Siegall cautioned investors that the initial increase in usage might not continue at the same rate:

It takes time to build market share in a setting where the standard of care hasn't changed in 40 years. I mean, it just takes time, and we are off to a good start. Our commercial team was ready. They were ready. They jumped on this, and we got the rapid adopters in. But the rest of the time, we're going to be making stepwise moves up there.

Management is guiding for third-quarter Adcetris sales in the range of $130million to $135million, a 6.2% to 10.3% quarter-over-quarter increase.

The next growth opportunity for Adcetris will come from mature T-cell lymphoma in a clinical trial called Echelon-2, which is scheduled to read out early in the fourth quarter. The number of potential patients with mature T-cell lymphoma is about the same as frontline Hodgkin lymphoma, but the current treatment isn't particularly good. So it may be easier to get rapid adoption in mature T-cell lymphoma if the Echelon-2 results show Adcetris is substantially better than the current standard of care.

Brian Orelli has no position in any of the stocks mentioned. The Motley Fool recommends Seattle Genetics. The Motley Fool has a disclosure policy.

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Seattle Genetics' Latest Approval Is the Best Yet -- The ...

Gene Screen BC 2011 Participant.18 Things You Should Know About Genetics is an animated film that presents fundamental background information about genetics, as well as offering some quirky but interesting facts about DNA, genes and genetics. It was created to be an upbeat, fun educational short film to initiate and draw interest to this sometimes daunting and seemingly complex subject matter.

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18 Things You Should Know About Genetics - YouTube

A recent1 review paper proposed a controversial claimthat the vast majority of animal species arose contemporary with modern humans. Not surprisingly, this claim was met with backlash from the evolutionary community. On what basis did the authors make this wide-reaching claim? Is their assertion true? Furthermore, what ramifications do their data have for the creationist explanation of the origin of species from the originally created min or kinds?

The main focus of Stoeckle and Thalers paper is genetics. Specifically, they focus on a subset of DNA in human and animal cells, termed mitochondrial DNA (mtDNA). Their analysis of mtDNA is clear, straightforward, and carefully justifiedso much so that I will summarize their arguments by liberally quoting from their paper.

About 15 years ago, DNA barcoding was first proposed as a tool for practical taxonomy.2 Taxonomy is the field of science concerned with the classification of life, and scientists thought that taking small subsets of DNA would aid in identifying and classifying species. The particular mitochondrial sequence that has become the most widely used is the 648 base pair (bp) [think of base pairs as DNA letters] segment of the gene [a subsection of DNA sequence] encoding mitochondrial cytochrome c oxidase subunit I (COI).3

With a subset of a subset of DNA, Skeptics of COI barcoding raised a number of objections about its power and/or generality as a single simple metric applicable to the entire animal kingdom, including: the small fraction of the genome (about 5% of the mitochondrial genome and less than one millionth of the total organisms genome [total DNA in an organism]) might not be sensitive or representative.4

A simple example from humans illustrates this concern. For instance, on average any two humans differ at 0.2%0.5% of their mtDNA base pairs. Theoretically, if all mtDNA differences are evenly distributed around the human mtDNA genome, you would expect 12 mtDNA differences in each individuals 648 bp COI barcode. With numbers this low, one generation of an extra mutation or two in the COI barcode sequence might throw a real classification pattern (i.e., one based on comparisons of hundreds of anatomical and physiological features) into confusion.

However, since the early days of DNA barcoding, such objections have been mostly mollified. I can attest to this from my own experience in handling thousands of mtDNA sequences. As a representative of the mtDNA diversity among species and individuals, a subset of mtDNA sequence is a good first approximation. Though subsets arent always perfect representations of the whole sequence, they are good initial data points.

Furthermore, over several decades of mtDNA barcoding, scientists have discovered a specific clustering pattern among mtDNA barcodes from individuals across diverse species: a general observation is that barcode clusters correspond best to species in well-studied animal groups, where taxonomists have mostly decided and agreed upon what species are. Thus there is good support in several major phyla, including Chordata [e.g., vertebrates and a handful of other species], Arthropoda [e.g., insects, arachnids, and crustaceans], Mollusca [e.g., shellfish, octopi], Echinodermata [e.g., starfish]. We note that these phyla are estimated to contain about 34 of named animal species.5

This fact has two major ramifications: First, the cluster structure of the animal world found in COI barcode analysis is independent of any definition(s) of species. Second, domain experts judgments of species tend to agree with barcode clusters and many apparent deviations turn out to be exceptions that prove the rule.6 In other words, the initial fears of those skeptical of DNA barcoding have not been met. Instead, barcoding has been very successful.

In light of these successes, the authors acknowledge the unexpected implications for explanations for the origin of species: At its origin DNA barcoding made no claim of contributing to evolutionary theory,7 yet the pattern of DNA barcode variance is the central fact of animal life that needs to be explained by evolutionary theory.8

Expanding our scope beyond the narrow evolutionary focus of the authors, we can generalize their statement: These mtDNA barcode patterns need to be explained by any model purporting to account for the origin of species.

The barcode patterns take a very specific form: the clustering structure of COI barcodessmall variance within species and often but not always sequence gaps among nearest neighbor species is the primary fact that a model of evolution and speciation must explain. Furthermore, the average pairwise difference among individuals (APD; equivalent to population genetics parameter ) within animal species is between 0.0% and 0.5%. The most data are available for modern humans, who have an APD of 0.1% calculated in the same way as for other animals.9

Stoeckle and Thaler recognize the sweeping potential in these patterns: The agreement of barcodes and domain experts implies that explaining the origin of the pattern of DNA barcodes would be in large part explaining the origin of species. Understanding the mechanism by which the near-universal pattern of DNA barcodes comes about would be tantamount to understanding the mechanism of speciation.10

In their evolutionary model, Stoeckle and Thaler invoke two hypotheses account for the barcode cluster patterns: Either 1) COI barcode clusters represent species-specific adaptations, OR 2) extant populations have recently passed through diversity-reducing regimes whose consequences for sequence diversity are indistinguishable from clonal bottlenecks.11

Their conclusion? Modern human mitochondria and Y chromosome [another subset of DNA, but inherited paternally] originated from conditions that imposed a single sequence on these genetic elements between 100,000 and 200,000 years ago.12 In other words, to account for human CO barcode patterns, they favor the second hypothesissome sort of population dynamic (contraction) that reduced the genetic diversity of the population.

Stoeckle and Thaler then extrapolate their conclusions to controversial heights. To justify their extrapolation, they caution that one should not as a first impulse seek a complex and multifaceted explanation for one of the clearest, most data rich and general facts in all of evolution. Then they draw a parallel: The simple hypothesis is that the same explanation offered for the sequence variation found among modern humans applies equally to the modern populations of essentially all other animal species. Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 200,000 years.13 In other words, based on mtDNA barcodes, Stoeckle and Thaler claim that the vast majority of species have originated contemporary with modern humans.

Though Stoeckle and Thaler dont perform this step, lets revisit their data and take their results to the next logical conclusion. We can do this because creationists have no problems with the observations that Stoeckle and Thaler describe. Ive already mentioned that my own experience with mtDNA matches theirsbarcodes are a useful first approximation and should be treated as such. Yet this first approximation has revealed a consistent patternlow numbers of mtDNA differences within species and higher numbers of mtDNA differences between species.

Furthermore, since Stoeckle and Thaler explore the origin of individual speciesrather than the origin of whole classification groups, like mammalstheir reasoning applies almost seamlessly to the creationist explanation for the origin of species. Their claim that species arose recently is one that focuses on species within kindsnot one that explores changes from one kind into another. In other words, for Stoeckle and Thalers particular question, evolutionists and creationists agree on the question of common ancestry.

Nevertheless, they differ sharply on the question of timewhen these individual species arose. Unlike Stoeckle and Thaler, creationists invoke not two, but three potential explanations for low numbers of mtDNA sequence differences within species: (1) species-specific adaptations; (2) changing population sizes or past bottlenecks (see especially the discussion of American bison (Bison bison) mtDNA and African buffalo (Syncerus caffer) mtDNA in this paper; (3) time recent origin (e.g., within the last 4,5006,000 years).

We now have two decades worth of direct measurements of the rate at which human mtDNA mutates, and it matches exactly the 6,000-year timescale and rejects the evolutionary timescale (see Genetics Confirms the Recent, Supernatural Creation of Adam and Eve and references therein). Thus, taking Stoeckle and Thalers results to their logical conclusion, we can revise their statement to Modern human [mitochondrial DNA] originated from conditions that imposed a single sequence on these genetic elements14 about 6,000 years ago.

Lets now re-extrapolate these results to other species. The simple hypothesis is that the same explanation offered for the sequence variation found among modern humans applies equally to the modern populations of essentially all other animal species. Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 6,000 years.

We can refine this conclusion even more, with more spectacular implications for the creationist model: In the last two decades, the mtDNA mutation rate in a handful of invertebrate species has also been directly measured, and these rates14 are around 10 times higher (or more!) than the human mtDNA mutation rate (again, see this article and references therein). This would imply that multiple species within a genus (or perhaps even a family) have originated within the last 6,000 years.

In other words, these broad mtDNA barcode results suggest that, in general, the predictions15 I made for mtDNA mutation rates in diverse species are likely to be fulfilled. This is good evidence that Darwins ideas are well on their way to being replaced.

As this article was going to press, the theistic evolutionary organization BioLogos posted a critique of Stoeckle and Thalers paper. More specifically, BioLogos posted a critique of creationist responses to Stoeckle and Thaler. BioLogos took strong exception to the type of thesis that I advanced above. For example, consider the following quote from BioLogos: "Did Stoeckel [sic] and Thaler conclude that 90% of animal species appeared at same time as humans? The answer is No [emphasis theirs].

Did I miss a key element of the Stoeckle and Thaler paper?

Lets take a look at the BioLogos article, which was written by PhD biologist and professor Joel Duff. Duff clearly desired to minimize the implications of Stoeckle and Thalers paper. For example, Duff characterized the journal in which it was published as a low-profile Italian journal. He also downplayed the impact, saying that the extended press release didnt generate much reaction inside or outside of the scientific community. More strongly, Duff denounced claims like the one I made above as mischaracterization of the original research. He said it was an incorrect claim that most species originated about the same time.

Why?

To support his assertion, Duff proposed an examination of the original intent of the authors of this paper. Since an authors intent is invisible unless the author clearly states it, Duffs suggested methodology to justify his strong critique is a creative way to tackle a scientific controversy.

After examining Stoeckle and Thalers intent to Duffs satisfaction, Duffs journalism gets more questionable. Weve already examined his emphatic assertion: Did Stoeckel [sic] and Thaler conclude that 90% of animal species appeared at same time as humans? The answer is No. Duff justifies his forceful condemnation with a quote from Stoeckle and Thalers paper: the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 200,000 years.16 In light of this quote, Duff concludes, In other words, the genetic diversity observed in mitochondrial genomes of most species alive today can be attributed to the accumulation of mutations from an ancestral genome within the past 200,000 years, and Duff asserts that the authors never claim that most species came into existence within the past 200,000 years.

For a critique that began with a proposal to examine intent, Duff seems to have missed the actual intent of the authors. The title of their paper is, Why should mitochondria define species? After discussing and justifying at length the observation that mtDNA differences do, in fact, delineate species, the authors then make a startling statement: The pattern of DNA barcode variance is the central fact of animal life that needs to be explained by evolutionary theory17 [emphasis theirs]. In case the intent of their statement wasnt transparent, the authors make it explicit: The agreement of barcodes and domain experts implies that explaining the origin of the pattern of DNA barcodes would be in large part explaining the origin of species. Understanding the mechanism by which the near-universal pattern of DNA barcodes comes about would be tantamount to understanding the mechanism of speciation.18 They then spend the next chunk of their paper discussing what mtDNA barcodes imply about the mechanism of speciation. Clearly, Stoeckle and Thaler are concerned with much more than just the accumulation of mutations from an ancestral genome within the past 200,000 years. Instead, they have a strong focus on the origin of species.

But did the authors never claim that most species came into existence within the past 200,000 years? In one sense, if we split hairs, Duff is technically correct: In their paper, Stoeckle and Thaler never say so explicitly. Yet as weve just observed, the conclusion about the timing of the origin of species is implied. Furthermore, Thaler makes the conclusion explicit in the press releasethe very one that Duff cited:

Our paper strengthens the argument that the low variation in the mitochondrial DNA of modern humans also explains the similar low variation found in over 90% of living animal specieswe all likely originated by similar processes and most animal species are likely young19. [emphasis added]

How did Biologos miss this?

Duff advances a second argument in his critique of the implications of Stoeckle and Thalers paper. He says that the mtDNA results at best, [tell] us the minimum age of the species. It tells us little to nothing about the maximum age of a species [emphasis his]. For the maximum age, Duff thinks the fossil record is essential. Furthermore, he states that an examination of the mitochondrial genome of any species will only tell us when the common ancestor of all modern members of this species existed, which will almost invariably occur after the evolutionary origin of the species.

But how does Duff know that this is true? Ive already documented that fossils do not directly record genealogical relationships; only DNA does. Why would Duff defer the genealogical question of ancestry (a.k.a. the question of the origin of species) to an indirect field of science (paleontology) when a direct field (geneticsmtDNA) gives a clear answer?

Ive also documented that the process of speciation involves several stepsat a minimum, (1) the formation of one or more distinct individuals, (2) the multiplication of these distinct individuals into a population, and (3) the isolation of this distinct population from the parent species. How does Duff know that the supposed ancestors (recorded by fossils) of modern species were isolated enough from the other populations alive at the time to be called a new species? Duff is trying to win a scientific argument, not by data and by experimentation, but by assertion. This is not a scientific way to resolve the controversy.

BioLogos response is sad, if not ironic. Weve already documented the fact that our evolutionary opponents dont read our literature (Duff included , despite BioLogos professed commitment to dialogue with those who hold other views); yet they call us liars. Sometimes I wonder if they carefully read even the evolutionary literature. Either way, BioLogos main critique (of the implications of Stoeckle and Thalers paper) amounts to misrepresentation and speculation even approaching outright denial. If this is the best that the evolutionary community can do, then perhaps my scientific conclusions (above) are even stronger than they first appear.

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Hundreds of Thousands of Species in a Few Thousand Years?