I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay.
Chị Võ Thị Hồng Nhật là người VN đầu tiên xuất bản 2 cuốn Cẩm Nang Sinh trắc dấu vân tay để phục vụ cho người dân Việt Nam có thêm công cụ tìm hiểu và khám phá bản thân.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay, và đã đăng ký bảo hộ sở hữu trí tuệ tại Việt Nam phần mềm Scientific Talents Analysia Việt hóa số 7124/2016/QTG.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay, và đã đăng ký bảo hộ sở hữu trí tuệ tại Việt Nam phần mềm Scientific Talents Analysia Việt hóa số 7124/2016/QTG.
Chị Võ Thị Hồng Nhật là người VN đầu tiên xuất bản 2 cuốn Cẩm Nang Sinh trắc dấu vân tay để phục vụ cho người dân Việt Nam có thêm công cụ tìm hiểu và khám phá bản thân.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay, và đã đăng ký bảo hộ sở hữu trí tuệ tại Việt Nam phần mềm Scientific Talents Analysia Việt hóa số 7124/2016/QTG.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay.
Chị Võ Thị Hồng Nhật là người VN đầu tiên xuất bản 2 cuốn Cẩm Nang Sinh trắc dấu vân tay để phục vụ cho người dân Việt Nam có thêm công cụ tìm hiểu và khám phá bản thân.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay, và đã đăng ký bảo hộ sở hữu trí tuệ tại Việt Nam phần mềm Scientific Talents Analysia Việt hóa số 7124/2016/QTG.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay, và đã đăng ký bảo hộ sở hữu trí tuệ tại Việt Nam phần mềm Scientific Talents Analysia Việt hóa số 7124/2016/QTG.
Chị Võ Thị Hồng Nhật là người VN đầu tiên xuất bản 2 cuốn Cẩm Nang Sinh trắc dấu vân tay để phục vụ cho người dân Việt Nam có thêm công cụ tìm hiểu và khám phá bản thân.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay, và đã đăng ký bảo hộ sở hữu trí tuệ tại Việt Nam phần mềm Scientific Talents Analysia Việt hóa số 7124/2016/QTG.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay.
I-Talents đã giúp hàng ngàn người Việt Nam tiếp cận công nghệ này,Và tất cả mọi người đã vô cùng hài lòng với nền tảng công nghệ của Giáo Sư Lin Jui Pin. Bằng sáng chế của Gs Lin được Mỹ cấp chứng nhận từ năm 2008, mã sáng chế US7406186. Một công nghệ phân tích vô cùng TUYỆT VỜI và đã được I-Talents ứng dụng hơn 6 năm nay.
892018 South Universityhttpsmyclasses.southuniversity.docxransayo
8/9/2018 South University
https://myclasses.southuniversity.edu/d2l/le/content/34297/viewContent/1114063/View 1/1
Download: Video Transcript (PDF 18KB) (media/week1/SU_W1_L1.pdf?
_&d2lSessionVal=X4ZxS4reQPabhOYfLa2QhfkZb&ou=34297)
The Scienti c Method
Biology consists of a great deal of knowledge. Much of that knowledge takes the form of facts that we
refer to as theories. Or perhaps this is better understood by saying that biologists treat theories as
though they were facts. But, they are special kind of fact. They are not a fact the way your social
security number is a fact. A theory is a fact that has been derived using the scienti c method.
The scienti c method always starts with an observation. And notice carefully that we use the singular
word, observation, and not the plural 'observations', even if a thousand events were observed. The
observation leads to a question. Questions come in many shapes and forms, but the scienti c method
needs to pose only very speci c questions. This is because the question must be able to be worded as a
hypothesis. What is a hypothesis? A hypothesis is a speci c statement in which a cause and effect
scenario is central. For an example, follow along with the scenarios presented in the assigned textbook
readings. You will see that a hypothesis can never be an open ended question. It must be speci c. For
example, this is a hypothesis: If I put a cover over a ame, it will go out. This is not a hypothesis: Why
does the ame go out when I put a cover over it? After you have created a hypothesis, you design
experiments to see if you can support your hypothesis. Keep in mind that in the biological sciences,
while you can support a hypothesis, you can never prove one. This is one of the most misunderstood
concepts in science. You will never account for every possible condition for a given hypothesis;
therefore, you can never prove it beyond any shadow of doubt.
https://myclasses.southuniversity.edu/content/enforced/34297-2405986/media/week1/SU_W1_L1.pdf?_&d2lSessionVal=X4ZxS4reQPabhOYfLa2QhfkZb&ou=34297
CHAPTER 5
Smith, T. M., & Smith, R. L. (2015). Elements of Ecology (9th ed.). Boston, MA: Pearson.
5.1 Adaptations Are a Product of Natural Selection
Stated more precisely, natural selection is the differential success (survival and reproduction) of individuals within the population that results from their interaction with their environment. As outlined by Darwin, natural selection is a product of two conditions: (1) that variation occurs among individuals within a population in some “heritable” characteristic, and (2) that this variation results in differences among individuals in their survival and reproduction as a result of their interaction with the environment. Natural selection is a numbers game. Darwin wrote:
Among those individuals that do reproduce, some will leave more offspring than others. These individuals are considered more fit than the others because they contribute the most to the next g.
Essay on Thermal Pollution | Thermal Pollution Essay for Students and .... Thermal Pollution Essay Example | StudyHippo.com. Thermal Pollution Essay | Essay on Thermal Pollution for Kids. Thermal pollution assignment - 2351 Words - NerdySeal. SOLUTION: write Essay on pollution - Studypool. Principle of Pollution Essay | Essay on Principle of Pollution for .... Pollution and Its Effects Essay | Essay on Pollution and Its Effects .... Thermal Pollution Research. Essay on Pollution For Students And Children | Pollution Essay 300 Words. Essays on Pollution | Types, Causes & Impacts Of Pollution. Thermal pollution. Thermal pollution short essay - cardiacthesis.x.fc2.com. Remarkable Pollution Essay ~ Thatsnotus. School essay: Essay writing effects of pollution. THERMAL POLLUTION. PPT - PRESENTATION ON POLLUTION PowerPoint Presentation, free download .... Thermal Pollution. 012 Essay Example Cause And Effect On Pollution ~ Thatsnotus. Essay on Pollution | Pollution Essay for Students and Children in .... Essay On Pollution And Its Causes – Telegraph. Essay on Thermal Pollution - House Fire Books. Thermal Pollution: Sources, Effects, Impacts and How to Control.
Life-Span Human Development 9th Edition Sigelman Solutions ManualTimothyPadilla
Full download : https://alibabadownload.com/product/life-span-human-development-9th-edition-sigelman-solutions-manual/
Life-Span Human Development 9th Edition Sigelman Solutions Manual
Lab 12 Building Phylogenies Objectives .docxDIPESH30
Lab 12
Building Phylogenies
Objectives
In this laboratory exercise, you will examine six species of agaricomycetes and predict the evolutionary
relationships among them. After completing this exercise you will be able to
• define ancestral characteristics, derived characteristics, branch point, and phylogeny.
• predict ancestral and derived characteristics for agaricomycetes.
• construct a phylogeny (phylogenetic tree).
• support the phylogeny with data.
• explain how evolutionary biologists discover evolutionary relationships.
Introduction
One of the most compelling pieces of evidence for evolution is that organisms have amazing similarities. An
example that almost everyone has heard before is that the limbs of birds, bats, horses, moles, cats, frogs,
humans, turtles, and other vertebrates have virtually the same skeletal plan. Furthermore, even snakes and
whales show structural remnants of the limbs of their ancestors. The evolutionary interpretation of these
similarities is that the vertebrate limb has been modified by natural selection to perform different functions
(for example, running, digging, flying). Another commonly used example is that the embryos of turtles,
mice, humans, chickens, and many other vertebrates are amazingly similar. Furthermore, the proteins and
DNA of organisms are remarkably similar. Why, do you suppose, can human diabetics use insulin extracted
from pigs to control their blood sugar levels? Well, the reason is that the chemical structure of human and
pig insulin is very similar.
In addition to these similarities, we discover that organisms that appear similar in one respect are often
similar in other respects (we can say the patterns are “concordant”). For example, organisms that are
similar morphologically (in shape) have similar protein structures. Organisms that are less similar
morphologically have less similar protein structures. This pattern holds for traits that are not easily
modified by evolution, but not so often by traits that are easily modified by selection. For example, flower
color might not be a good trait to use when looking for concordance because it is easily changed
genetically.
The concordance of traits is an important support of evolution. Imagine that we saw that organisms similar
in one set of characteristics were very different in a second set of characteristics and different again in a
third set of characteristics. This situation would be chaotic and we would be forced to question the reality
1
of evolution. The development of methods of DNA and protein analysis has shown dramatically that
organisms that are similar morphologically are also similar at the genetic level.
So, similarity among organisms provides evidence for evolution. We can then turn around and use the
similarities to try to reconstruct evolutionary relationships. That is the purpose of today’s lab: to construct a
hypothes ...
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1- Why was the Tomasetti et al article so misinterpreted by thAgripinaBeaulieuyw
1- Why was the Tomasetti et al article so misinterpreted by the media? Draw from
your own personal experiences to discuss other scientific phenomenon that has
been similarly misinterpreted.
2- What might be the consequences of scientific misreporting of this article?
3- What is the overall value of the Tomasetti et al paper? Cite two and be specific in
your rational for selecting these reasons.
4- Cite three criticisms of this paper. Be specific in the rationale for your criticism.
5- Design an experiment which might distinguish between environmental effects
and replicative errors in canter etiology.
You may assume you have access to all resources currently available to scientists
today,
Be specific in elucidating the application of the scientific method to your
experiment:
1) Observation
2) Hypothesis
3) Predictions
4) Experiment: Independent and dependent variables, controls, uncontrolled
variables, sample size
5) Results (predicted): How would you analyze your data
6)Conclusions: predict conclusions for the various outcomes of your experiment
REPORT
◥
CANCER ETIOLOGY
Stem cell divisions, somatic
mutations, cancer etiology, and
cancer prevention
Cristian Tomasetti,1,2* Lu Li,2 Bert Vogelstein3*
Cancers are caused by mutations that may be inherited, induced by environmental
factors, or result from DNA replication errors (R). We studied the relationship between
the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries
throughout the world. The data revealed a strong correlation (median = 0.80) between
cancer incidence and normal stem cell divisions in all countries, regardless of their
environment. The major role of R mutations in cancer etiology was supported by an
independent approach, based solely on cancer genome sequencing and epidemiological
data, which suggested that R mutations are responsible for two-thirds of the mutations
in human cancers. All of these results are consistent with epidemiological estimates of the
fraction of cancers that can be prevented by changes in the environment. Moreover, they
accentuate the importance of early detection and intervention to reduce deaths from the
many cancers arising from unavoidable R mutations.
I
t is now widely accepted that cancer is the
result of the gradual accumulation of driver
gene mutations that successively increase cell
proliferation (1–3). But what causes these muta-
tions? The role of environmental factors (E)
in cancer development has long been evident
from epidemiological studies, and this has fun-
damental implications for primary prevention.
The role of heredity (H) has been conclusively
demonstrated from both twin studies (4) and the
identification of the genes responsible for cancer
predisposition syndromes (3, 5). We recently hy-
pothesized that a third source—mutations due to
the random mistakes made during normal DNA
replication (R)—can explain why cancers occur
much more commonly in som ...
1- Why was the Tomasetti et al article so misinterpreted by thsachazerbelq9l
1- Why was the Tomasetti et al article so misinterpreted by the media? Draw from
your own personal experiences to discuss other scientific phenomenon that has
been similarly misinterpreted.
2- What might be the consequences of scientific misreporting of this article?
3- What is the overall value of the Tomasetti et al paper? Cite two and be specific in
your rational for selecting these reasons.
4- Cite three criticisms of this paper. Be specific in the rationale for your criticism.
5- Design an experiment which might distinguish between environmental effects
and replicative errors in canter etiology.
You may assume you have access to all resources currently available to scientists
today,
Be specific in elucidating the application of the scientific method to your
experiment:
1) Observation
2) Hypothesis
3) Predictions
4) Experiment: Independent and dependent variables, controls, uncontrolled
variables, sample size
5) Results (predicted): How would you analyze your data
6)Conclusions: predict conclusions for the various outcomes of your experiment
REPORT
◥
CANCER ETIOLOGY
Stem cell divisions, somatic
mutations, cancer etiology, and
cancer prevention
Cristian Tomasetti,1,2* Lu Li,2 Bert Vogelstein3*
Cancers are caused by mutations that may be inherited, induced by environmental
factors, or result from DNA replication errors (R). We studied the relationship between
the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries
throughout the world. The data revealed a strong correlation (median = 0.80) between
cancer incidence and normal stem cell divisions in all countries, regardless of their
environment. The major role of R mutations in cancer etiology was supported by an
independent approach, based solely on cancer genome sequencing and epidemiological
data, which suggested that R mutations are responsible for two-thirds of the mutations
in human cancers. All of these results are consistent with epidemiological estimates of the
fraction of cancers that can be prevented by changes in the environment. Moreover, they
accentuate the importance of early detection and intervention to reduce deaths from the
many cancers arising from unavoidable R mutations.
I
t is now widely accepted that cancer is the
result of the gradual accumulation of driver
gene mutations that successively increase cell
proliferation (1–3). But what causes these muta-
tions? The role of environmental factors (E)
in cancer development has long been evident
from epidemiological studies, and this has fun-
damental implications for primary prevention.
The role of heredity (H) has been conclusively
demonstrated from both twin studies (4) and the
identification of the genes responsible for cancer
predisposition syndromes (3, 5). We recently hy-
pothesized that a third source—mutations due to
the random mistakes made during normal DNA
replication (R)—can explain why cancers occur
much more commonly in som ...
1- Why was the Tomasetti et al article so misinterpreted by th.docxjeremylockett77
1- Why was the Tomasetti et al article so misinterpreted by the media? Draw from
your own personal experiences to discuss other scientific phenomenon that has
been similarly misinterpreted.
2- What might be the consequences of scientific misreporting of this article?
3- What is the overall value of the Tomasetti et al paper? Cite two and be specific in
your rational for selecting these reasons.
4- Cite three criticisms of this paper. Be specific in the rationale for your criticism.
5- Design an experiment which might distinguish between environmental effects
and replicative errors in canter etiology.
You may assume you have access to all resources currently available to scientists
today,
Be specific in elucidating the application of the scientific method to your
experiment:
1) Observation
2) Hypothesis
3) Predictions
4) Experiment: Independent and dependent variables, controls, uncontrolled
variables, sample size
5) Results (predicted): How would you analyze your data
6)Conclusions: predict conclusions for the various outcomes of your experiment
REPORT
◥
CANCER ETIOLOGY
Stem cell divisions, somatic
mutations, cancer etiology, and
cancer prevention
Cristian Tomasetti,1,2* Lu Li,2 Bert Vogelstein3*
Cancers are caused by mutations that may be inherited, induced by environmental
factors, or result from DNA replication errors (R). We studied the relationship between
the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries
throughout the world. The data revealed a strong correlation (median = 0.80) between
cancer incidence and normal stem cell divisions in all countries, regardless of their
environment. The major role of R mutations in cancer etiology was supported by an
independent approach, based solely on cancer genome sequencing and epidemiological
data, which suggested that R mutations are responsible for two-thirds of the mutations
in human cancers. All of these results are consistent with epidemiological estimates of the
fraction of cancers that can be prevented by changes in the environment. Moreover, they
accentuate the importance of early detection and intervention to reduce deaths from the
many cancers arising from unavoidable R mutations.
I
t is now widely accepted that cancer is the
result of the gradual accumulation of driver
gene mutations that successively increase cell
proliferation (1–3). But what causes these muta-
tions? The role of environmental factors (E)
in cancer development has long been evident
from epidemiological studies, and this has fun-
damental implications for primary prevention.
The role of heredity (H) has been conclusively
demonstrated from both twin studies (4) and the
identification of the genes responsible for cancer
predisposition syndromes (3, 5). We recently hy-
pothesized that a third source—mutations due to
the random mistakes made during normal DNA
replication (R)—can explain why cancers occur
much more commonly in som ...
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ATH 2100READING (Simple” Mendelian Inheritance)DIRECTIONS P.docxjaggernaoma
ATH 2100 READING (“Simple” Mendelian Inheritance)
DIRECTIONS: Please read the materials that follow and then complete Quiz 6 on PILOT.
By the time you finish reading these materials, you should be able to answer the following questions:
1. What is the difference between a simple and a complex trait?
2. What similarities do simple and complex traits share?
3. Are most human traits simple or complex?
4. What distinguishes a genotype from a phenotype?
5. What are the genetic versus non-genetic factors that influence complex traits?
In this week’s lab, you will examine variation in Mendelian traits with your classmates. From this information, you will determine the phenotypes and potential genotypes found in our classroom. Put simply, a phenotype is a physical trait that we can observe (e.g., presence of a widow’s peak or absence of mid-digital hair). Some people will call phenotypes “variants” or “traits” so pay attention when these words are used in class! The phenotype is controlled in large part by the genotype, which is the genetic composition of an organism, represented by pairs of alleles (e.g., AA, Aa, or aa). As an example, the genotype “aa”might control for the phenotype “dimples,” while the genotypes AA and Aa control for the phenotype “no dimples.”
SIMPLE AND COMPLEX TRAITS
Mendelian(or “simple”) traits are traits that exhibit a simple inheritance pattern with a limited amount of genetic and phenotypic variation. Mendelian traits, therefore, are controlled for by a single genetic locus and are physically expressed as traits that are usually either present or absent. Simple traits tend not to be influenced by the environment because they are not major contributors to natural selection (in which the environment is a key element).
Non-Mendelian (or “complex”) traits are traits that follow an inheritance pattern in which the genotype sets the genetic “potential” for a trait, while the physical and cultural environment impacts how the phenotype will be expressed (i.e., what you will look like, do, etc.). Close to 100% of HUMAN traits are inherited in a complex fashion, which makes it difficult for researchers to determine the underlying causes leading people to behave and even respond to treatment for diseases in different ways.
Simple inheritance can be easily tracked by looking at phenotypes- as you will learn in class, Mendel used the phenotypic differences in the shape and color of pea plant flowers, pea plant leaves, pea pods, and the peas inside the pods to track simple inheritance patters. On the other hand, complex inheritance patterns require much more sophisticated methods for locating genetic differences because the combination of allele pairs is only ONE part of what gives you your phenotype. In this week’s lab you will explore several “simple traits” like earlobe shape and the ability to roll your tongue.
The reality is that almost all of these traits have since been shown to be “complex” traits- but, th.
Why is it important to study reactions norms to understand phenotypi.pdfarrowmobile
Why is it important to study reactions norms to understand phenotypic plasticity?
Solution
Ans:
Phenotypic plasticity, the capacity of a single genotype to exhibit variable phenotypes in
different environments, is common in insects and is often highly adaptive. Phenotypic plasticity
is important because it expands the existing “genocentric” evolutionary theory, producing an
encompassing paradigm to explain life on earth. Plasticity was once considered “noise” but is
now widely recognized as potentially adaptive under a wide array of circumstances. As with any
major shift in scientific thinking, phenotypic plasticity engenders new ideas, causing us to ask
new questions and test hypotheses that would not otherwise be examined, leading us to
productive new scientific insights.
Phenotypic plasticity is counterbalance to mutation driven evolution: It is not surprising that
during the first half of the 20th Century, scientists, flushed with excitement about Mendelian
genetics, viewed evolution primarily as a mutational process. However, this bias largely ignored
an important reality of evolution – that natural selection selects not among genotypes, but among
phenotypes. Thus, the phenotype, and variation among phenotypes, plays a major role in
evolution. And, because the environment in which an individual develops determines its
phenotype, the environment also assumes a greater role in evolution, and may, in fact, produce
more viable phenotypic variation than do mutations. This is because mutations are not only rare,
but usually deleterious. In contrast, a single environmental factor may alter the phenotypes of an
entire population, providing natural selection with access to perhaps thousands of
environmentally altered individuals, as opposed to a single mutant individual. In addition,
mutations generally arise randomly with no correlation to specific environments, whereas new
environmentally induced phenotypes are both directional and highly correlated with the specific
new environment, allowing new environments to immediately produce and select among new
phenotypes.
Including phenotypic plasticity produces a better model: As suggested above, the inclusion of
phenotypic plasticity can result in a better model than mutation-allelic substitution alone in
explaining the production of organismal diversity. For example, the initial evolution of warning
color (aposematism), starting as a rare mutation is problematic because conspicuous prey should
be quickly found and removed by predators (Lindström et al. 2001). In contrast, evolution of
aposematism is easily explained by phenotypic plasticity (Sword 2002). Likewise, for
development, phenotypic plasticity explains the evolution of allometry and exaggerated
morphologies (Emlen and Nijhout 2000, Shingleton et al. 2007). For physiology, phenotypic
plasticity explains adaptive, beneficial plasticities such as acclimation and response to exercise
(Swallow et al. 2005), quite well. In ecology, it aids our un.
GENETICS & MALOCCLUSION - II /orthodontic courses by Indian dental academy Indian dental academy
Description :
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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The Stroop EffectEffect18TitleStudent’s NamePro.docxsarah98765
The Stroop Effect Effect 18
Title
Student’s Name
Professor’s Name
Course
Date
Abstract
The Stroop effect is a phenomenon in cognitive psychology with numerous applications. This phenomenon occurs when an individual is given a task of identifying the color of a word rather the word itself. The concept behind this experiment is simplified although the reaction time when there is a mismatch in the color and word represents an integral study in cognitive psychology. The basic operation of the Stroop effect is to relatively measure the concentration and power of the mind. It would be easier for an individual to name the color of a word in a similar color. This means that a normal mind finds it simpler to name a color with matching sematic meaning in wording. Generally, Stroop effect measures the correlation between interference and reaction time. The first development of the Stroop effect was demonstrated in 1935 by an American psychologist named John Ridley Stroop. From his original experiment, different psychological hypothesis have been drawn. Topping to this is the development of numerous articles explaining, experimenting or expounding on this effect. The articles have been strongly based on Stroop’s original effect although different researchers have replicated his effect.
The initial experiment has been discussed in many psychological classes. Researchers in the field of experimental psychology have cited the original paper in their various studies. The application of Stroop effect in clinical practice has aided in finding treatment for patients with psychological disorders. The Stroop effect is also imperative in investigations since it acts as a feasible psychological test. Experimental findings from different tests reveal stimuli reaction due to sematic interference and sematic facilitation. Stroop conceptual framework secludes three stimuli groups (incongruent, neutral and congruent).The stimuli are used during all experiments to draw conclusions. The Stroop effect is processes within two parts of the brain; the dorsolateral prefrontal cortex and the anterior cingulate cortex. Results from reaction to stimuli in the two brain parts are explained using a number of theories namely; selective attention, processing speed, parallel distributed processing and automacity. The Stroop effect has been a milestone in collating cognitive development with other variables viz. working memory and processing speed. Researchers have published modified Stroop tests in bilingualism. In this field, wrapped words, reverse tests and spatial tests have all been applied.
Introduction
Macleod empties Stroop effect as one of the most popular study in cognitive science and psychology. In its basic application, the test entails ignoring a printed word then naming the color of the word. Basically naming the color printed in a word such as BLUE is surrounded by many cognitive properties. Automacity was introduced in 1886 since it is easier to read word as c.
My thesis in Computational Ecology was carried under the supervision of Prof. Ronen Kadmon, and submitted on Dec 2013 to the senate of the Hebrew University in Jerusalem.
892018 South Universityhttpsmyclasses.southuniversity.docxransayo
8/9/2018 South University
https://myclasses.southuniversity.edu/d2l/le/content/34297/viewContent/1114063/View 1/1
Download: Video Transcript (PDF 18KB) (media/week1/SU_W1_L1.pdf?
_&d2lSessionVal=X4ZxS4reQPabhOYfLa2QhfkZb&ou=34297)
The Scienti c Method
Biology consists of a great deal of knowledge. Much of that knowledge takes the form of facts that we
refer to as theories. Or perhaps this is better understood by saying that biologists treat theories as
though they were facts. But, they are special kind of fact. They are not a fact the way your social
security number is a fact. A theory is a fact that has been derived using the scienti c method.
The scienti c method always starts with an observation. And notice carefully that we use the singular
word, observation, and not the plural 'observations', even if a thousand events were observed. The
observation leads to a question. Questions come in many shapes and forms, but the scienti c method
needs to pose only very speci c questions. This is because the question must be able to be worded as a
hypothesis. What is a hypothesis? A hypothesis is a speci c statement in which a cause and effect
scenario is central. For an example, follow along with the scenarios presented in the assigned textbook
readings. You will see that a hypothesis can never be an open ended question. It must be speci c. For
example, this is a hypothesis: If I put a cover over a ame, it will go out. This is not a hypothesis: Why
does the ame go out when I put a cover over it? After you have created a hypothesis, you design
experiments to see if you can support your hypothesis. Keep in mind that in the biological sciences,
while you can support a hypothesis, you can never prove one. This is one of the most misunderstood
concepts in science. You will never account for every possible condition for a given hypothesis;
therefore, you can never prove it beyond any shadow of doubt.
https://myclasses.southuniversity.edu/content/enforced/34297-2405986/media/week1/SU_W1_L1.pdf?_&d2lSessionVal=X4ZxS4reQPabhOYfLa2QhfkZb&ou=34297
CHAPTER 5
Smith, T. M., & Smith, R. L. (2015). Elements of Ecology (9th ed.). Boston, MA: Pearson.
5.1 Adaptations Are a Product of Natural Selection
Stated more precisely, natural selection is the differential success (survival and reproduction) of individuals within the population that results from their interaction with their environment. As outlined by Darwin, natural selection is a product of two conditions: (1) that variation occurs among individuals within a population in some “heritable” characteristic, and (2) that this variation results in differences among individuals in their survival and reproduction as a result of their interaction with the environment. Natural selection is a numbers game. Darwin wrote:
Among those individuals that do reproduce, some will leave more offspring than others. These individuals are considered more fit than the others because they contribute the most to the next g.
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Life-Span Human Development 9th Edition Sigelman Solutions ManualTimothyPadilla
Full download : https://alibabadownload.com/product/life-span-human-development-9th-edition-sigelman-solutions-manual/
Life-Span Human Development 9th Edition Sigelman Solutions Manual
Lab 12 Building Phylogenies Objectives .docxDIPESH30
Lab 12
Building Phylogenies
Objectives
In this laboratory exercise, you will examine six species of agaricomycetes and predict the evolutionary
relationships among them. After completing this exercise you will be able to
• define ancestral characteristics, derived characteristics, branch point, and phylogeny.
• predict ancestral and derived characteristics for agaricomycetes.
• construct a phylogeny (phylogenetic tree).
• support the phylogeny with data.
• explain how evolutionary biologists discover evolutionary relationships.
Introduction
One of the most compelling pieces of evidence for evolution is that organisms have amazing similarities. An
example that almost everyone has heard before is that the limbs of birds, bats, horses, moles, cats, frogs,
humans, turtles, and other vertebrates have virtually the same skeletal plan. Furthermore, even snakes and
whales show structural remnants of the limbs of their ancestors. The evolutionary interpretation of these
similarities is that the vertebrate limb has been modified by natural selection to perform different functions
(for example, running, digging, flying). Another commonly used example is that the embryos of turtles,
mice, humans, chickens, and many other vertebrates are amazingly similar. Furthermore, the proteins and
DNA of organisms are remarkably similar. Why, do you suppose, can human diabetics use insulin extracted
from pigs to control their blood sugar levels? Well, the reason is that the chemical structure of human and
pig insulin is very similar.
In addition to these similarities, we discover that organisms that appear similar in one respect are often
similar in other respects (we can say the patterns are “concordant”). For example, organisms that are
similar morphologically (in shape) have similar protein structures. Organisms that are less similar
morphologically have less similar protein structures. This pattern holds for traits that are not easily
modified by evolution, but not so often by traits that are easily modified by selection. For example, flower
color might not be a good trait to use when looking for concordance because it is easily changed
genetically.
The concordance of traits is an important support of evolution. Imagine that we saw that organisms similar
in one set of characteristics were very different in a second set of characteristics and different again in a
third set of characteristics. This situation would be chaotic and we would be forced to question the reality
1
of evolution. The development of methods of DNA and protein analysis has shown dramatically that
organisms that are similar morphologically are also similar at the genetic level.
So, similarity among organisms provides evidence for evolution. We can then turn around and use the
similarities to try to reconstruct evolutionary relationships. That is the purpose of today’s lab: to construct a
hypothes ...
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1- Why was the Tomasetti et al article so misinterpreted by thAgripinaBeaulieuyw
1- Why was the Tomasetti et al article so misinterpreted by the media? Draw from
your own personal experiences to discuss other scientific phenomenon that has
been similarly misinterpreted.
2- What might be the consequences of scientific misreporting of this article?
3- What is the overall value of the Tomasetti et al paper? Cite two and be specific in
your rational for selecting these reasons.
4- Cite three criticisms of this paper. Be specific in the rationale for your criticism.
5- Design an experiment which might distinguish between environmental effects
and replicative errors in canter etiology.
You may assume you have access to all resources currently available to scientists
today,
Be specific in elucidating the application of the scientific method to your
experiment:
1) Observation
2) Hypothesis
3) Predictions
4) Experiment: Independent and dependent variables, controls, uncontrolled
variables, sample size
5) Results (predicted): How would you analyze your data
6)Conclusions: predict conclusions for the various outcomes of your experiment
REPORT
◥
CANCER ETIOLOGY
Stem cell divisions, somatic
mutations, cancer etiology, and
cancer prevention
Cristian Tomasetti,1,2* Lu Li,2 Bert Vogelstein3*
Cancers are caused by mutations that may be inherited, induced by environmental
factors, or result from DNA replication errors (R). We studied the relationship between
the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries
throughout the world. The data revealed a strong correlation (median = 0.80) between
cancer incidence and normal stem cell divisions in all countries, regardless of their
environment. The major role of R mutations in cancer etiology was supported by an
independent approach, based solely on cancer genome sequencing and epidemiological
data, which suggested that R mutations are responsible for two-thirds of the mutations
in human cancers. All of these results are consistent with epidemiological estimates of the
fraction of cancers that can be prevented by changes in the environment. Moreover, they
accentuate the importance of early detection and intervention to reduce deaths from the
many cancers arising from unavoidable R mutations.
I
t is now widely accepted that cancer is the
result of the gradual accumulation of driver
gene mutations that successively increase cell
proliferation (1–3). But what causes these muta-
tions? The role of environmental factors (E)
in cancer development has long been evident
from epidemiological studies, and this has fun-
damental implications for primary prevention.
The role of heredity (H) has been conclusively
demonstrated from both twin studies (4) and the
identification of the genes responsible for cancer
predisposition syndromes (3, 5). We recently hy-
pothesized that a third source—mutations due to
the random mistakes made during normal DNA
replication (R)—can explain why cancers occur
much more commonly in som ...
1- Why was the Tomasetti et al article so misinterpreted by thsachazerbelq9l
1- Why was the Tomasetti et al article so misinterpreted by the media? Draw from
your own personal experiences to discuss other scientific phenomenon that has
been similarly misinterpreted.
2- What might be the consequences of scientific misreporting of this article?
3- What is the overall value of the Tomasetti et al paper? Cite two and be specific in
your rational for selecting these reasons.
4- Cite three criticisms of this paper. Be specific in the rationale for your criticism.
5- Design an experiment which might distinguish between environmental effects
and replicative errors in canter etiology.
You may assume you have access to all resources currently available to scientists
today,
Be specific in elucidating the application of the scientific method to your
experiment:
1) Observation
2) Hypothesis
3) Predictions
4) Experiment: Independent and dependent variables, controls, uncontrolled
variables, sample size
5) Results (predicted): How would you analyze your data
6)Conclusions: predict conclusions for the various outcomes of your experiment
REPORT
◥
CANCER ETIOLOGY
Stem cell divisions, somatic
mutations, cancer etiology, and
cancer prevention
Cristian Tomasetti,1,2* Lu Li,2 Bert Vogelstein3*
Cancers are caused by mutations that may be inherited, induced by environmental
factors, or result from DNA replication errors (R). We studied the relationship between
the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries
throughout the world. The data revealed a strong correlation (median = 0.80) between
cancer incidence and normal stem cell divisions in all countries, regardless of their
environment. The major role of R mutations in cancer etiology was supported by an
independent approach, based solely on cancer genome sequencing and epidemiological
data, which suggested that R mutations are responsible for two-thirds of the mutations
in human cancers. All of these results are consistent with epidemiological estimates of the
fraction of cancers that can be prevented by changes in the environment. Moreover, they
accentuate the importance of early detection and intervention to reduce deaths from the
many cancers arising from unavoidable R mutations.
I
t is now widely accepted that cancer is the
result of the gradual accumulation of driver
gene mutations that successively increase cell
proliferation (1–3). But what causes these muta-
tions? The role of environmental factors (E)
in cancer development has long been evident
from epidemiological studies, and this has fun-
damental implications for primary prevention.
The role of heredity (H) has been conclusively
demonstrated from both twin studies (4) and the
identification of the genes responsible for cancer
predisposition syndromes (3, 5). We recently hy-
pothesized that a third source—mutations due to
the random mistakes made during normal DNA
replication (R)—can explain why cancers occur
much more commonly in som ...
1- Why was the Tomasetti et al article so misinterpreted by th.docxjeremylockett77
1- Why was the Tomasetti et al article so misinterpreted by the media? Draw from
your own personal experiences to discuss other scientific phenomenon that has
been similarly misinterpreted.
2- What might be the consequences of scientific misreporting of this article?
3- What is the overall value of the Tomasetti et al paper? Cite two and be specific in
your rational for selecting these reasons.
4- Cite three criticisms of this paper. Be specific in the rationale for your criticism.
5- Design an experiment which might distinguish between environmental effects
and replicative errors in canter etiology.
You may assume you have access to all resources currently available to scientists
today,
Be specific in elucidating the application of the scientific method to your
experiment:
1) Observation
2) Hypothesis
3) Predictions
4) Experiment: Independent and dependent variables, controls, uncontrolled
variables, sample size
5) Results (predicted): How would you analyze your data
6)Conclusions: predict conclusions for the various outcomes of your experiment
REPORT
◥
CANCER ETIOLOGY
Stem cell divisions, somatic
mutations, cancer etiology, and
cancer prevention
Cristian Tomasetti,1,2* Lu Li,2 Bert Vogelstein3*
Cancers are caused by mutations that may be inherited, induced by environmental
factors, or result from DNA replication errors (R). We studied the relationship between
the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries
throughout the world. The data revealed a strong correlation (median = 0.80) between
cancer incidence and normal stem cell divisions in all countries, regardless of their
environment. The major role of R mutations in cancer etiology was supported by an
independent approach, based solely on cancer genome sequencing and epidemiological
data, which suggested that R mutations are responsible for two-thirds of the mutations
in human cancers. All of these results are consistent with epidemiological estimates of the
fraction of cancers that can be prevented by changes in the environment. Moreover, they
accentuate the importance of early detection and intervention to reduce deaths from the
many cancers arising from unavoidable R mutations.
I
t is now widely accepted that cancer is the
result of the gradual accumulation of driver
gene mutations that successively increase cell
proliferation (1–3). But what causes these muta-
tions? The role of environmental factors (E)
in cancer development has long been evident
from epidemiological studies, and this has fun-
damental implications for primary prevention.
The role of heredity (H) has been conclusively
demonstrated from both twin studies (4) and the
identification of the genes responsible for cancer
predisposition syndromes (3, 5). We recently hy-
pothesized that a third source—mutations due to
the random mistakes made during normal DNA
replication (R)—can explain why cancers occur
much more commonly in som ...
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
ATH 2100READING (Simple” Mendelian Inheritance)DIRECTIONS P.docxjaggernaoma
ATH 2100 READING (“Simple” Mendelian Inheritance)
DIRECTIONS: Please read the materials that follow and then complete Quiz 6 on PILOT.
By the time you finish reading these materials, you should be able to answer the following questions:
1. What is the difference between a simple and a complex trait?
2. What similarities do simple and complex traits share?
3. Are most human traits simple or complex?
4. What distinguishes a genotype from a phenotype?
5. What are the genetic versus non-genetic factors that influence complex traits?
In this week’s lab, you will examine variation in Mendelian traits with your classmates. From this information, you will determine the phenotypes and potential genotypes found in our classroom. Put simply, a phenotype is a physical trait that we can observe (e.g., presence of a widow’s peak or absence of mid-digital hair). Some people will call phenotypes “variants” or “traits” so pay attention when these words are used in class! The phenotype is controlled in large part by the genotype, which is the genetic composition of an organism, represented by pairs of alleles (e.g., AA, Aa, or aa). As an example, the genotype “aa”might control for the phenotype “dimples,” while the genotypes AA and Aa control for the phenotype “no dimples.”
SIMPLE AND COMPLEX TRAITS
Mendelian(or “simple”) traits are traits that exhibit a simple inheritance pattern with a limited amount of genetic and phenotypic variation. Mendelian traits, therefore, are controlled for by a single genetic locus and are physically expressed as traits that are usually either present or absent. Simple traits tend not to be influenced by the environment because they are not major contributors to natural selection (in which the environment is a key element).
Non-Mendelian (or “complex”) traits are traits that follow an inheritance pattern in which the genotype sets the genetic “potential” for a trait, while the physical and cultural environment impacts how the phenotype will be expressed (i.e., what you will look like, do, etc.). Close to 100% of HUMAN traits are inherited in a complex fashion, which makes it difficult for researchers to determine the underlying causes leading people to behave and even respond to treatment for diseases in different ways.
Simple inheritance can be easily tracked by looking at phenotypes- as you will learn in class, Mendel used the phenotypic differences in the shape and color of pea plant flowers, pea plant leaves, pea pods, and the peas inside the pods to track simple inheritance patters. On the other hand, complex inheritance patterns require much more sophisticated methods for locating genetic differences because the combination of allele pairs is only ONE part of what gives you your phenotype. In this week’s lab you will explore several “simple traits” like earlobe shape and the ability to roll your tongue.
The reality is that almost all of these traits have since been shown to be “complex” traits- but, th.
Why is it important to study reactions norms to understand phenotypi.pdfarrowmobile
Why is it important to study reactions norms to understand phenotypic plasticity?
Solution
Ans:
Phenotypic plasticity, the capacity of a single genotype to exhibit variable phenotypes in
different environments, is common in insects and is often highly adaptive. Phenotypic plasticity
is important because it expands the existing “genocentric” evolutionary theory, producing an
encompassing paradigm to explain life on earth. Plasticity was once considered “noise” but is
now widely recognized as potentially adaptive under a wide array of circumstances. As with any
major shift in scientific thinking, phenotypic plasticity engenders new ideas, causing us to ask
new questions and test hypotheses that would not otherwise be examined, leading us to
productive new scientific insights.
Phenotypic plasticity is counterbalance to mutation driven evolution: It is not surprising that
during the first half of the 20th Century, scientists, flushed with excitement about Mendelian
genetics, viewed evolution primarily as a mutational process. However, this bias largely ignored
an important reality of evolution – that natural selection selects not among genotypes, but among
phenotypes. Thus, the phenotype, and variation among phenotypes, plays a major role in
evolution. And, because the environment in which an individual develops determines its
phenotype, the environment also assumes a greater role in evolution, and may, in fact, produce
more viable phenotypic variation than do mutations. This is because mutations are not only rare,
but usually deleterious. In contrast, a single environmental factor may alter the phenotypes of an
entire population, providing natural selection with access to perhaps thousands of
environmentally altered individuals, as opposed to a single mutant individual. In addition,
mutations generally arise randomly with no correlation to specific environments, whereas new
environmentally induced phenotypes are both directional and highly correlated with the specific
new environment, allowing new environments to immediately produce and select among new
phenotypes.
Including phenotypic plasticity produces a better model: As suggested above, the inclusion of
phenotypic plasticity can result in a better model than mutation-allelic substitution alone in
explaining the production of organismal diversity. For example, the initial evolution of warning
color (aposematism), starting as a rare mutation is problematic because conspicuous prey should
be quickly found and removed by predators (Lindström et al. 2001). In contrast, evolution of
aposematism is easily explained by phenotypic plasticity (Sword 2002). Likewise, for
development, phenotypic plasticity explains the evolution of allometry and exaggerated
morphologies (Emlen and Nijhout 2000, Shingleton et al. 2007). For physiology, phenotypic
plasticity explains adaptive, beneficial plasticities such as acclimation and response to exercise
(Swallow et al. 2005), quite well. In ecology, it aids our un.
GENETICS & MALOCCLUSION - II /orthodontic courses by Indian dental academy Indian dental academy
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The Stroop EffectEffect18TitleStudent’s NamePro.docxsarah98765
The Stroop Effect Effect 18
Title
Student’s Name
Professor’s Name
Course
Date
Abstract
The Stroop effect is a phenomenon in cognitive psychology with numerous applications. This phenomenon occurs when an individual is given a task of identifying the color of a word rather the word itself. The concept behind this experiment is simplified although the reaction time when there is a mismatch in the color and word represents an integral study in cognitive psychology. The basic operation of the Stroop effect is to relatively measure the concentration and power of the mind. It would be easier for an individual to name the color of a word in a similar color. This means that a normal mind finds it simpler to name a color with matching sematic meaning in wording. Generally, Stroop effect measures the correlation between interference and reaction time. The first development of the Stroop effect was demonstrated in 1935 by an American psychologist named John Ridley Stroop. From his original experiment, different psychological hypothesis have been drawn. Topping to this is the development of numerous articles explaining, experimenting or expounding on this effect. The articles have been strongly based on Stroop’s original effect although different researchers have replicated his effect.
The initial experiment has been discussed in many psychological classes. Researchers in the field of experimental psychology have cited the original paper in their various studies. The application of Stroop effect in clinical practice has aided in finding treatment for patients with psychological disorders. The Stroop effect is also imperative in investigations since it acts as a feasible psychological test. Experimental findings from different tests reveal stimuli reaction due to sematic interference and sematic facilitation. Stroop conceptual framework secludes three stimuli groups (incongruent, neutral and congruent).The stimuli are used during all experiments to draw conclusions. The Stroop effect is processes within two parts of the brain; the dorsolateral prefrontal cortex and the anterior cingulate cortex. Results from reaction to stimuli in the two brain parts are explained using a number of theories namely; selective attention, processing speed, parallel distributed processing and automacity. The Stroop effect has been a milestone in collating cognitive development with other variables viz. working memory and processing speed. Researchers have published modified Stroop tests in bilingualism. In this field, wrapped words, reverse tests and spatial tests have all been applied.
Introduction
Macleod empties Stroop effect as one of the most popular study in cognitive science and psychology. In its basic application, the test entails ignoring a printed word then naming the color of the word. Basically naming the color printed in a word such as BLUE is surrounded by many cognitive properties. Automacity was introduced in 1886 since it is easier to read word as c.
My thesis in Computational Ecology was carried under the supervision of Prof. Ronen Kadmon, and submitted on Dec 2013 to the senate of the Hebrew University in Jerusalem.
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2. 130 Dermatoglyphics
Contents
Introduction....................................................................................................................130
Materials ........................................................................................................................130
Notes for the Instructor..................................................................................................131
Student Outline ..............................................................................................................133
Literature Cited..............................................................................................................140
Appendices A to C.........................................................................................................141
Introduction
All too often when we teach genetics we limit ourselves to the "tried and true" single gene traits
and "shy away" from more complex forms of genetic inheritance. After all, it is difficult enough to
explain Mendelian Laws without the added complexity of quantitative variation. Ironically,
understanding the relationship between genetic information and phenotypic expression at the
organismal level has more to do with the interaction of many genes than it does to any one gene in
isolation. Dermal ridges are an example of a trait that shows quantitative variation, is inherited, and
is easily analyzed in the teaching laboratory. Further, sophisticated mathematical treatments need
not be applied to teach the relationship between polygenic inheritance and expression.
The Student Outline is intended for students in an introductory genetics course. However, the
exercise is easily adaptable to a beginning biology course and could even be shortened to less than
one full laboratory period. The adaptability is possible by selectively eliminating one or more
aspects of the laboratory experience. As written here, this exercise requires about 2–3 hours to
complete. By deleting the statistical analysis of palm prints and using the Down Syndrome prints as
demonstration, the exercise can be completed in less than 1 hour.
Materials
There are two methods for obtaining prints both of which will work adequately. This exercise is
written for use with the inking method. Porolon ink pads can be obtained from: Sirchie Finger Print
Laboratories, Umstead Industrial Park, P.O. Box 30576, Raleigh, NC 27612, (919) 781-3120. The
cost, as of July 1989, is $19.50 US each (catalog no. FPT267). An alternative would be to purchase
ink ($5.75/4 oz), a roller (FPT262A, 3 inches wide, $8.95), and supply your own surface (glass or
steel); 2- and 4-inch rollers are also available.
I do not recommend using office-type ink pads. The ink is too thin and does not consistently
yield high quality prints. Also, it is very difficult to remove from your hands once it has dried.
An alternative method is to use three-quarter inch clear plastic tape for fingerprints and 4-inch
wide clear plastic tape for palm prints. Graphite powder (available from many chemical supply
companies) is rubbed over the area to be printed and the tape is gently pressed against the surface.
When the tape is peeled off an image of the print will be transferred to the tape which can then be
pressed onto a sheet of paper. The 4-inch tape, known as Book-Lock, can be obtained in 20-yard
rolls from: Library Store, P.O. Box 964, 112 E. South St., Tremont, IL 61568, (800) 548-7204. One
roll will service about 40 students and costs $7.99 US (or less if purchased in bulk).
3. Dermatoglyphics 131
Other supplies for each student include a protractor (to measure the ATD angle) and a dissecting
microscope (for making ridge counts). Also, the master copies of the Down Syndrome prints can be
attached to clear plastic sheets so that students can mark them using felt-tip pens.
Notes for the Instructor
Dermatoglyphics and Development
Dermal ridges originate from fetal volar pads composed of mesenchymal tissue starting at the
sixth to seventh week of development. The size and position of the volar pads are largely
responsible for ridge patterns observed. In general, small pads produce arches and larger pads
produce loops or whorls. Lateral displacement of the volar pad creates asymmetry of the pattern.
Ridges become visible at about 3 months and are completed by the sixth month of prenatal
development.
It has been postulated (see Schaumann and Alter, 1976) that ridges are influenced by blood
vessel-nerve pairs at the border between the dermis and epidermis during prenatal development.
Features such as inadequate oxygen supply, abnormal nerve growth, unusual patterning or
distribution of sweat glands, alterations of epithelial growth, or other features could influence ridge
patterns. Because growth is a dynamic process, one in which many components contribute and can
mutually interact, there must be many genes involved.
Holt (1968) has demonstrated a very close correspondence between the observed and predicted
correlation for total ridge count (TRC) and the degree of genetic relatedness. That is, TRC acts as
an additive genetic trait with little dominance deviation. TRC is a near perfect fit to the classic
polygenic model in which one assumes that each gene "adds" in some small way to the total
observed variability. But what is being "added"? Clearly, a phenotypic expression which requires a
multitude of tissue types, all simultaneously growing and changing as development proceeds, is at
odds with a simplistic image of genes being somehow "additive." The resolution to this dilemma is
to recognize that the additive model was never intended to be physically real to any organism. It is
simply a functional mathematical tool that relates genotype to phenotype in a global sense. Put
another way, understanding additive genetic variability gives you predictive ability about the
phenotypes you might see in future generations but does not tell you anything about the underlying
biology. Why is this distinction important? Because it is critical that undergraduates understand the
context and the complexity of the genotype-phenotype relationship beyond just focusing on the
statistical aspects of quantitative inheritance.
For another example of teaching applications using dermatoglyphics see Mendenhall et al.
(1989). A good overview of dermatoglyphics with clinical interpretations can be found in Reed
(1981).
Thought Questions for Use in Class
1. Since dermal ridge patterns are fixed for life, does that mean there is no environmental effect?
Depends on what you mean by the environment. Although the basic pattern and ridge count
does not change as you age, scars can distort a pattern and heavy manual labor can wear them down.
2. If all 10 fingers derive by mitosis and share a common set of genetic information (totipotency),
why don't they all look the same?
4. 132 Dermatoglyphics
Prenatally, there appears to be several components influencing growth fields of ridge counts.
Roberts (1979) argues for at least four major induction factors: (1) some feature which influences
the overall ridge count, (2) another that increases ridge counts more on the radial than the ulnar side
of the finger, (3) an increase in ridge counts more on the radial than ulnar side of the hand, and (4)
an additional positive radial effect for the index finger and to a lesser extent on the thumb. Roberts
(1979:488) concludes that "each finger [acts] as a different point in relation to others in the
multidimensional space produced by these factors." Put another way, each finger is a different
microenvironment of development.
3. If the left and right hands are both the products of a common genotype, why is there often a
different ridge pattern for the same finger of each hand?
Although there is a genetic component to ridge patterns, it is not purely deterministic. There
must be stochastic effects during development that influence ridge patterns.
4. If we were to look at the dermatoglyphic patterns and ridge counts of identical twins would they
be absolutely identical?
Identical twins share extremely similar dermatoglyphic patterns. However, there are usually
small, but detectable differences between them. This is a further confirmation that dermatoglyphic
patterns and counts are under genetic control and also influenced by stochastic effects.
5. What effect does the maternal environment have?
Correlations between mother/child and father/child for TRC are similar suggesting that maternal
the environment is not influential.
6. Why are dermatoglyphic patterns altered with Down Syndrome?
The presence of the extra chromosome dramatically alters prenatal development and can have
varying effects on each organ system. Generally, the nervous system is the most sensitive of the
organ systems during prenatal development and characteristically leads to mental retardation for
those with Down Syndrome. Not surprisingly, a trait such as ridge patterning which is influenced
by induction fields, positioning of the volar pads, and nerve-vessel pairing would be affected in
some complex, perhaps mutually interacting, fashion.
7. If Down Syndrome is a genetic trait caused by an extra chromosome 21, why is there individual
variation in the ridge pattern and ATD angle?
One would not expect an identical phenotypic outcome because each individual inherits a
unique set of genetic information that also influences expression in addition to the overall effect
produced by the extra chromosome.
8. Given that Down Syndrome affects many organ systems during prenatal development, should
not other chromosomal defects alter dermal ridges for the same reason?
5. Dermatoglyphics 133
Yes. Altered patterns are known, for example, for trisomy 18, trisomy 13, XXX, XXY, and an
assortment of duplications and deletions to name just a few.
9. If nerve-vessel pairing influences ridge patterning, should not abnormalities of these specific
tissues affect dermal ridges?
Ridge aplasia is a rare autosomal dominant condition. No dermal ridges are formed on the
hands or feet, a condition probably caused by a failure of nerves to grow into the epithelium during
prenatal development. Many serious congenital defects result in abnormal dermatoglyphic patterns
termed ridge dysplasia (perhaps caused by deviations in the normal nerve branching) or ridge
distortion (likely the result of a disturbance in the spatial arrangements of nerves). These clinical
cases serve to demonstrate the multiplicity of effects (pleiotropism) a genetic condition can produce.
Student Outline
The study of ridged skin, dermatoglyphics, was pioneered by Sir Francis Galton in the late 19th
century. Since that time, extensive work has been carried out on the biology and genetics of skin
patterns. You will analyze fingerprint patterns, the total ridge count, and ATD angles among
members of the class and investigate dermatoglyphic differences found on individuals having Down
Syndrome (trisomy 21).
Fingerprint Patterns
Dermatoglyphic patterns are due to the convoluted layers of cells of the epidermis. At the peak
of the ridges are found the pores of the sweat glands (see Figure 8.1). Ridges are laid during
embryonic growth and remain unchanged during postnatal development. However, extensive
physical labor can wear them down and scars can distort the pattern.
Figure 8.1 The detailed structure of dermal ridges.
6. 134 Dermatoglyphics
There are three major classes of fingerprints: arches, loops and whorls (see Figure 8.2). Loops
can be defined as radial or ulnar. Ulnar loops open towards the little finger and radial loops open
towards the thumb. A useful descriptive term in dermatoglyphics is the triradius. A triradius is a
point of convergence for three regions that separate almost parallel ridges. Loops have one triradius
(on the thumb side if ulnar and towards the little finger if radial) and whorls have two. Arches lack
a triradius.
Figure 8.2. The three main types of fingerprint patterns. Whorls have two triradii, loops have
one, and arches none.
The genetics of fingerprint patterns is not well established. Based on one large pedigree, single
gene control was deduced for certain patterns (Slatis et al., 1976). The lack of confirmation from
other investigators and the cautious presentation of these results by the authors suggests that this
scheme is tentative and awaits the test of time. Slatis and his colleagues suggest that all ulnar loops
are the baseline pattern and that certain genes modify this phenotype. They also suggest that
epistasis between loci may play a role. Table 8.1 is adapted from the work of Slatis et al. (1976).
Total Ridge Counts
A ridge count is made by drawing a line from the triradius to the center of the pattern and
determining the number of intersected ridges between these two points (see Figure 8.3). Arches are
defined as having a ridge count of zero. The ridge count of a whorl consists of the higher of the two
counts. A total ridge count (TRC) is the summation of the ridge count for all 10 fingers. Other
important considerations are quoted from Holt (1968:40):
"The triradius is not included in the count, nor is the final ridge when it forms the center of the
pattern. Ridges which run close to the line without meeting it are excluded, but two ridges resulting
from a bifurcation are both counted. It is usual to exclude from the count the fine secondary
intervening ridges which occur occasionally, chiefly on thumbs. These secondary intervening
ridges do not carry sweat gland pores. Furthermore, they are not as high as other ridges and whether
or not they appear on a print depends on the degree of pressure exerted when the print is made. It is
possible, therefore, to have two prints of the same finger, one showing secondary ridges and the
other not. Islands, on the other hand, are always counted."
7. Table 8.1. The inheritance of fingerprint patterns.
Effect Inheritance Genotypes Phenotypes
Thumb Semidominant AA whorls, both thumbs
Aa 2 ulnar loops or
1 ulnar loop and 1 whorl
aa ulnar loops, both thumbs
Thumb Dominant B- arches on thumbs and
often other fingers
Index finger Dominant C- radial loops on index
finger, often associated
with an arch on the
middle finger
Ring finger Semidominant CC whorls, both fingers
Cc 2 ulnar loops or
1 ulnar loop and 1 whorl
ulnar loops on both fingers
Ring or little finger Recessive dd radial loops
All fingers Dominant E whorls on all fingers except for
an ulnar
loop on middle finger
All fingers Dominant F–* arches on fingers
* may be more than one gene involved
The genetics of total ridge counts has revealed that there is considerable variation among
unrelated individuals, but there is a statistically significant positive correlation among relatives.
This means that closely related individuals are more likely to be similar than distantly related ones
due to the degree of shared genetic heritage. Detecting positive correlations among relatives is a
common approach for analyzing the genetic component of complex phenotypic traits. With this
method it is very difficult, if not impossible, to determine the number of contributing genes. It is
usually presumed that there are many genes controlling the overall phenotype (polygenes). Traits
such as total ridge count which have a range of phenotypic expression are called quantitative traits.
They are generally described in statistical terms (such as correlations) since the genotype is not
known. However, in one study of total ridge counts, it has been suggested that half of the variation
is controlled by a single locus (Spence et al., 1973). Possibly a number of other genes have some
small effect on the phenotype also.
8. Dermatoglyphics136
Figure 8.3 . The technique of ridge counting. This loop has a ridge count of 13.
Palm Prints
At the base of the palm, there are usually four triradii: a, b, c, and d (see Figure 8.4). An axial
triradius (t) is usually located near the point where the palm is connected to the wrist. Two percent
of normal individuals have this triradius positioned near the center of the palm (termed t′′). A
triradius found halfway in between these two positions (t′) is found on 21% of the normal
population. Approximately 11% of the population will have some combination of more than one
axial triradius.
A useful descriptive measure is the ATD angle formed by drawing a line from a to t and from d
to t. If there are multiple axial triradii, only the largest angle is considered. The ATD angle
averages 48° among normal individuals. People with Down Syndrome have an ATD angle
averaging 81°. Elevated ATD angles are also found on individuals with other forms of
chromosomal abnormalities including trisomy 18, trisomy 13, Klinefelter Syndrome (XXY), and
Turner Syndrome (XO). A wide range of unusual dermatoglyphic features other than the ATD
angle are also useful for recognizing genetic abnormalities. Dermatoglyphics is an especially quick
and simple diagnostic tool for newborns. It is important to point out that many anomalies produce
similar skin patterns so that corroboration with cytogenetic analysis or other appropriate tests is
essential.
Dermatoglyphics of Down Syndrome
In addition to the elevated ATD angle described above, several other features are also useful in
the diagnosis of Down Syndrome. These include:
1. Fingers with mostly ulnar loops (especially the index finger); radial loops on the ring and index
fingers.
9. Dermatoglyphics 137
Figure 8.4. A palm print showing the triradii and ATD angle.
2. A single flexion crease on the little finger. A flexion crease is the skin fold that occurs when
you bend your fingers.
3. Simian crease.
4. A loop between the base of the index and middle finger and/or the middle and ring fingers. The
loop opens to the inter-digital space.
5. Hypothenar ulnar loops, whorls, or carpal loops. The palm is roughly divided into two halves.
The thenar region on the thumb side and hypothenar on the little finger side. Carpal region refers to
the very base of the palm.
No one feature is diagnostic and many of these patterns are found in the normal population.
However, when several are present together, they are indicative of Down Syndrome. On the print
given to you look for the above mentioned traits. Because the Down prints vary in quality, it is not
possible to determine if all of these traits are present on any one individual.
How to Make Fingerprints and Palm Prints
To make good fingerprints, touch the ink with your finger on its side and roll smoothly across
the ink l80° to the opposite side of the finger and lift. Repeat the motion on paper, transferring the
print. It is easiest if you place the paper at the edge of the table to give your hand space to rotate.
You will find that sometimes the second or third print after inking yields a clearer image of the
ridges. Check the print to see if it is smudged. The triradii of loops and whorls must be visible.
Repeat as necessary.
Palm prints require a similar procedure. The palm needs to be slowly rolled to transfer the
edges. The a, t, and d triradii need to be visible. Remove ink from your hands with soap and water.
10. Dermatoglyphics138
Students' t test
The t test is a statistical procedure for comparing two means and will be used to detect a
difference, if any, between the ATD angles of the normal (classroom) population and that of the
Down population. Simply taking the difference between two means does not convey enough
information. A mean can be composed of numbers that are clustered together or very dispersed.
To make a comparison, there must be a measure of dispersion around the mean. This is
reflected in the variance—a value which is the average squared difference from the mean. In the
case of ATD angles, the variance is a pooled estimate of both the normal (classroom) and Down
Syndrome population. It is presumed that the variance is the same for both. Keep in mind that the
mean and variance are estimators; that is, they give an approximate value of the true population
mean and variance from the data at hand.
The variance, s2
, is:
Σ (x1i - 1)2
+ Σ (x2i - 2)2
s2
= (n = sample size)
n1 + n2 - 2
By rearrangement, the variance can be put in a form that is easier to use computationally:
Σ x1i
2
- (Σ x1i)2
/n1 + Σ x2i
2
- (Σ x2i)2
/n2
s2
=
n1 + n2 - 2
The square root of the variance (termed the standard deviation) is used in the calculation of the t-
value.
x1 - x2
t =
s (1/n1 + 1/n2)1/2
Notice that the difference between the means (numerator) is adjusted by the degree of variation
around the mean (denominator). If the denominator is small then division by a small number makes
the t-value large. Statistical differences are detected when the calculated t-value surpasses the
critical t-value in Table 8.2. The critical values establish a rejection level at P < 0.05 for the
appropriate degrees of freedom (degrees of freedom = n1 + n2 - 2).
If larger samples were available, the ability to detect a difference between two populations
would be improved. Inspection of the formula for the t-value reveals that as n1 and n2 become
larger, 1/n1 and 1/n2 become smaller. This has the effect of inflating the t-value and therefore
enhances the ability to detect small differences between means.
Drawing conclusions with a t test requires a probability statement. There is no assurance that
the conclusion is true; rather one argues that the statistical analysis supports a given outcome at a
particular probability level.
11. Dermatoglyphics 139
Table 8.2. Critical values of t.
Degrees of freedom Value of t Degrees of freedom Value of t
1 12.706 16 2.120
2 4.303 17 2.110
3 3.182 18 2.101
4 2.776 19 2.093
5 2.571 20 2.086
6 2.447 21 2.080
7 2.365 22 2.074
8 2.306 23 2.069
9 2.262 24 2.064
10 2.228 25 2.060
11 2.201 26 2.056
12 2.179 27 2.052
13 2.160 28 2.048
14 2.145 29 2.045
15 2.131 30 2.042
Procedure
1. Obtain a fingerprint pad and practice getting clear prints on a piece of scrap paper.
2. When you feel you have got the knack, make a set of prints on the data sheets.
3. Practice, then prepare palm prints on the data sheet.
4. To determine your genotype, classify your fingerprints according to the scheme by Slatis et al.
(1976).
5. Draw a line from the triradii to the center of the pattern and use a dissecting microscope to
determine the total ridge count (TRC).
6. Obtain class data for total ridge counts and make a histogram with 10 ridge intervals. A
quantitative trait often demonstrates a bell-shaped distribution if sufficient data points are available.
Is there a trend towards such a distribution?
7. Draw lines on your palm prints to form an ATD angle and determine the angle.
8. Obtain the class data for ATD angles. Your instructor will provide palm prints from Down
Syndrome individuals; determine the ATD angles and pool the class results. Do not write directly
on these prints; lay clear plastic over them and use the felt-tip pens provided.
9. Using only the data for the right hand, calculate the class mean and the mean for Down
Syndrome individuals. Use the left had print of Down Syndrome individuals if the right hand print
is not measurable. Perform a t test and determine if claims for a difference exist. Have your
analysis checked by your instructor.
12. Dermatoglyphics140
Literature Cited
Holt, S. B. l968. The genetics of dermal ridges. Thomas, Springfield, Illinois, 195 pages.
Mendenhall, G., T. Mertens, and J. Hendrix. 1989. Fingerprint ridge count. American Biology
Teacher, 51:203–207.
Reed, T. 1981. Dermatoglyphics in medicine: Problems and use in suspected chromosome
abnormalities. American Journal of Medical Genetics, 8:411–429.
Roberts, D. 1979. Dermatoglyphics and human genetics. Pages 475–494, in Dermatoglyphics –
Fifty years later (W. Wertelecki and C. C. Plato, Editors). Birth Defects: Original Article
Series, Vol. 15, No. 6, Alan R. Liss, New York, 800 pages.
Schaumann, B., and M. Alter. 1976. Dermatoglyphics in medical disorders. Springer-Verlag, New
York, 258 pages.
Slatis, H. M., M. B. Katznelson, and B. Bonne-Tamir. l976. The inheritance of fingerprint patterns.
American Journal of Human Genetics, 28:280–289.
Spence, M. A., R. C. Elston, K. K. Namboodiri, and W. S. Pollitzer. 1973. Evidence for a possible
major gene effect in absolute finger ridge count. Human Heredity, 23:414–421.
15. Dermatoglyphics 143
APPENDIX C
Left and Right Palm Prints from Six Down Syndrome Adults
Showing the Position of the ATD Angle
The figure on the following page serves as the instructor key to go along with the six full-size
prints provided on the succeeding pages. Above each hand is the fingerprint pattern established
from prints that were taken at the same time (UL = ulnar loop; RL = radial loop; and W = whorl).
Two fingerprints from the 28-year-old female were unreadable.
An adjunct to the Down Syndrome exercise would be to compare the frequency of pattern types
between the class and the Down Syndrome individuals, the latter typically showing a higher
frequency of ulnar loops.