Category: Genetics

Introduction

The author tries to prove the importance of facial attractiveness on genetic diversity. He therefore carries out a background research to make predictions and then undertakes an empirical research to prove his hypothesis. The study applies two approaches in its investigations.

The first approach that it applies to study the relationship between facial features and their genetic human preferences is the novel approach where the author tries to investigate whether attractiveness has any association with mate quality. The second approach which applies the use of microsatellite markers in an empirical approach, investigates the structural facial characteristics which can be used to determine the relationship between facial attractiveness and the relative genetic diversity.

Goals of the Research

The main aim of the author is to establish the significance of facial attractiveness in genetic diversity in terms of mate preferences. The author tries to establish whether males also have unique preference for Major Histocompatibility Complex (MHC) heterogygosity in female’s appearances.

This was prompted by research results which have proved that MHC genotype has an influence in mate preferences for many species. Another goal that the author tries to find out is whether genetic diversity is also associated with female facial attractiveness.

The author also tries to show the role of MHC in human beings as regards to mate preferences. The author investigates the differences between the influences of genetic diversity and the possible influences of MHC genetic diversity on humans’ mate preferences. MHC could be essential particularly in mate preferences since MHC heterozygosity had no correlation with the general heterozygosity in many human samples.

The author also tries to establish the relationship between human facial attractiveness and the genetic diversity that falls within as well as outside the MHC. Finally, the author investigates whether genetic diversity has any relationship with femininity, masculinity as well as averageness.

Hypotheses

The author predicts that there is a strong correlation between genetic diversity and facial attractiveness. The author also predicts that genetic diversity has a strong relationship with major histocompatibility complex and influences reproductive success and fitness. The author hypothesizes that facial characteristics shapes the selection for high-quality males.

Research Methodology

The research applied the use of microsatellite markers which is normally used to carry out researches on non-human animal studies to investigate the genetic significance of human facial attractiveness. The microsatellite markers are used in approximating the genetic diversity independently for non-MHC as well as MHC loci and in estimating the individual mean heterozygosity which the author symbolized by H as well as the standard mean which the author also symbolized as d2.

The study involved taking DNA samples from 160 Caucasian students from the University of Western Australia who had written consents for their participation in the research. 80 males and females took part respectively and their ages averaged at 20 and 19 in that order. The research procedures were endorsed by the Human Research Ethics Committee in the university.

Thereafter, DNA samples were taken and two Buccal swabs were collected from each participant. These were then set up for Polymerase Chain Reaction (PCR) under the instructions of the manufacturer. The Australian Genome Research Facility did the PCR as well as fragment analyses. 12 microsatellites were typed at key loci in the MHC region that had linkages with disequilibrium in every HLA locus.

In measuring the non-MHC genetic diversity, the researchers used eleven non-MHC microsatellites which were all from elevens different chromosomes. The MHC microsatellites as well as the non-MHC microsatellites chosen were qualitatively similar in terms of the number of alleles as well as the expected heterozygosity. Bayesian Clustering Method was to analyze the population ancestry for each participant (Donnley et al. 2000,).

Genetic diversity for non-MHC loci as well as for MHC loci was measured separately. This was done using standard mean d2, the individual mean heterozygosity (H) as well as genetic distance in the alleles. Both H and d2 were calculated at each locus per individual.

The d2 measure was standardized to achieve a higher weighting of every locus. The standardized values were averaged in all loci to achieve a standardized d2. There was also the need to test for the underlying mechanisms of the effects of the genetic diversity particularly on the facial appearance.

Here, Heterozygosity-heterozygosity (H-H) correlation test was used. It involved randomly sampling the loci into two sets where each set was examined to establish whether each H that was calculated from the two groups was correlated to the other.

The procedure was replicated 100 times, each time randomly resampling to achieve a standard deviation, a strong correlation coefficient and mean for MHC as well as non-MHC loci. Multiple regression models were applied to analyze each locus so as to determine the local effects of genetic diversity.

Quality digital color photograph was also taken of students who participated in the DNA sampling. The participants were asked to remove their make-ups or any facial hair before the photographs were taken. The researchers used separate groups from the same university mainly from the opposite sex to rate the attractiveness, masculinity, symmetry as well as averageness and femininity of each photograph. Outliers in the face ratings who had extreme scores below and above the mean and the standard deviations were removed.

Multiple regression models were then used to separately conduct male and female analysis. Pearson’s correlation coefficient was used to analyze face ratings: hierarchical multiple regression which included the use of SPSS 16 and Sobel’s test were used to analyze attractiveness.

Conclusion

The results of the study proved that MHC diversity has a critical effect on male facial attractiveness. It also proved that males’ and females’ particular attractive facial characteristics were related to their genetic diversity. It established that the MHC is responsible for female preferences for the facial attractiveness of the male. However, MHC plays no role in male preferences for the female’s facial attractiveness.

The study also provided evidence of the relationship between facial appearance and genetic diversity (Brown 1997; 1999). It also established that human facial attractiveness especially that of the male faces influenced the mate quality. Finally, the results showed that the males as well as the female are inclined at finding attractive genotype in the opposite sex faces. The author boasts of having provided research results that links MHC genotype with male facial averageness.

Critique

The strength of the study lies in its methodology. The author applies the use of novel approach to provide the basis for his predictions on the relationship between facial attractiveness and genetic diversity in humans. It tests variables which are practical and easy to test using the available research methodologies and analysis models. It tests attractiveness, masculinity, symmetry as well as femininity and averageness.

The various methods used in collecting the data, testing and analyzing the variables are standard and valid. Although microsatellite marker that was used has majorly been applied in other non-human animals, it was used perfectly used as the researchers sought the guide of the manufacturers of the Polymerase Chain Reaction (PCR).

The use of multiple regression models to analyze the variables makes the research more credible. The multiple regression models enable the researchers to present reliable qualitative results which also lead to stronger conclusive results. The results are explained qualitatively and supported by quantitative results of the empirical research.

According to the reviewer, the research failed to organize a sample size that could provide stronger results. The author acknowledges that there was a fairly small sample size for the research. Thus it was not possible to find significant relationship between attractiveness and the non-MHC standardized-mean.

The research could not provide significant statistical power to prove the relationship. Besides, the study has made use of all white Caucasians as the respondents. Perhaps if the research was a comparative study between say, the Caucasians and the African Americans, this would have helped to shed more light on the research.

The methods that were used in the research are certainly appropriate as they helped investigate the possible associations between genetics and attractiveness in human beings through DNA sampling and use of photographs.

According to the reviewer, the research method that was applied provided more conclusive results which could not have been possible through the use of another method. The previous results that had been done by other research methods could not establish MHC’s role in mate preferences as well as whether males had any unique preferences on the females’ facial attractiveness.

This research was the first to provide evidence on the role of MHC diversity on male facial attractiveness. It was also the first to establish that genetic diversity is related to unique facial attractiveness. This proves the feasibility and the credibility of the research. Therefore, in the reviewer’s opinion, this was the best research methodology for the research topic. However, the results presented could have been more comprehensive and stronger if he sample size could have been made larger and diverse.

Significance

The research makes significant contributions to the field of evolution. It provides evidences that support the relationship between genetics and human attractiveness. It enables us understand the underlying phenotypic characteristics which are associated with genotype in opposite-sex facial attractiveness, thus providing significant insights into human sexual selection. It enhances research in genetic diversity as it explores research areas which have never been proven by previous researches in the topic.

The topic of the study in the article is well covered in the study book used in class (Ridley 2004). The book covers many areas covered by the article and provides more insight in it since most of the contents of the article is related to several chapters and subtopics in the book. However, the research methodology used in the study; Microsatellite Markers, has not been fully elaborated in the book.

The research methodology has proved to be more reliable and therefore more skills on its application would be very important in our research processes. I would also recommend that Ridley (2004) cite this article since it presents a professionally conducted research with strong conclusions.

The evidences presented in the article have quantitative data to support them. The article would offer more credibility to the information provided in the “Quantitative Genetics” in chapter nine of the book (Ridley, 2004). The article provides relevant evidence to most sub topics in this chapter and this would offer learners and all those interested in the field of evolution a comprehensive learning material with more accurate and recent research results.

Follow-Up Design

The next level in the research should investigate the association of MHC-genotype and health. This would help justify the fact that genetic diversity has an effect on the reproductive success as well as fitness (Lie, Hanne and Simmons 2008).

In this case, the variables would be facial attractiveness, skin quality, masculinity, symmetry as well as averageness and femininity. The research would attempt to prove the fact put forward by Donnely et al (155), which explain that MHC heterozygous males have healthier skin as compared to less heterozygous males.

Therefore the hypothesis for the study would be: there is a strong correlation between MHC genotype and skin quality. The research methodology would involve the use of microsatellite in collecting DNA samples and in calculating the individual mean heterozygosity as well as standard mean for the DNA tests. Photographs would also be taken and analyzed by other separate groups from the non-participants. The results of all the tests carried out would then be quantitatively analyzed using multiple regression models.

Works Cited

Brown, Jerram. The new heterozygosity theory of mate choice and the MHC. Genetica, 104 (1999):215–221.

Brown, Jerram. A theory of mate choice based on heterozygosity. Behav. Ecol., 8(1997):60–65.

Donnely, Peter., Pritchard, Jonathan., and Stephens, Mathew. Inference of population structure using multilocus genotype data. Genetics, 2000(155): 945–959

Lie, Hanne., Simmons, Leigh., and Rhodes, Gillian. Genetic diversity revealed in human faces. Crawley: University of Western Australia, 2008. Print.

Ridley, Mark. Evolution. London: Wiley-Blackwell, 2004. Print.

Before the discovery of Mendelian genetics, Aristotle and Hippocrates supported the concept of blending inheritance in explaining how organisms inherit traits. The concept of blending inheritance holds that genetic traits of parents randomly combine and generate intermediate traits in their respective offspring. However, the emergence of Mendelian genetics has rendered the concept of blending inheritance erroneous due to its inability to explain the persistence of variations and intermittent occurrence of traits. Therefore, this essay explains why valid genetic concepts such as incomplete dominance, co-dominance, pleiotropy, epistasis, and polygenic traits support the erroneous concept of blending inheritance.

The concept of incomplete dominance in genetics explains a situation where the expression of one of a pair of alleles partially dominates or suppresses the other allele. In genetics, traits can either be dominant or recessive depending on their expression levels in organisms. In incomplete dominance, offspring acquire intermediate traits, which reflect the blend of different traits of the parents. For example, the cross between red-flowered and white-flowered pea plants results in the production of pink-flowered pea plants. Essentially, traits in red flowers partially dominate the traits in while flowers resulting in blended traits in pink flowers. In this view, incomplete dominance in genetics supports the concept of blending inheritance.

The concept of co-dominance in genetics elucidates a scenario where there is an equal expression of dominant or recessive genes resulting in the production of a combined trait. Co-dominance normally occurs when parents with dominant traits or recessive traits cross and give rise to offspring with dominant traits or recessive traits respectively. Moreover, the expression of the inherited dominant traits or recessive traits has equal strength in that neither trait can dominate the other. As dominant traits or recessive traits in organisms have equal strength of expression, they blend and confer traits that reflect both traits. For example, A and B are dominant traits of a blood group that equally blend to form the AB blood group. Thus, co-dominance supports the concept of blending inheritance in genetics.

The concept of pleiotropy in genetics explains a phenomenon where a single gene in an organism has multiple phenotypic traits, which are normally unrelated to the gene. Pleiotropy supports the concept of blending inheritance because it indicates that a single gene can have multiple phenotypes, which can only occur through blending with other genes and phenotypes. For instance, sickle cell anemia is a genetic abnormality that occurs due to the pleiotropic effects of the mutation in the gene that encodes for hemoglobin. Thus, the ability of a single gene to cause multiple phenotypic effects implies that genes can blend and generate blended traits.

Epistasis is a genetic concept that explains how genes can interact and influence phenotypic characteristics in an organism. Essentially, epistasis holds that one gene can mask or magnify the expression of another gene. For example, the gene for baldness interacts with genes for red hair and blond hair to cause complete baldness in an individual. In this view, the gene for red hair or the gene for blond hair magnifies the occurrence of complete baldness in an individual. Therefore, the ability of genes to interact shows that they can blend and generate blended phenotypes in line with the concept of blending inheritance.

Polygenic traits comprise traits that are subject to the expression of two or more genes in different gene loci. Polygenic traits emanate from a polygenic inheritance, which is a genetic concept that elucidates how numerous genes influence a given trait. The hair color is an example of a polygenic trait because it is under the influence of numerous genes in humans. Hence, the ability of numerous genes to influence a trait implies that genes blend and bring about unique traits, according to the concept of blending inheritance.

In conclusion, the genetic concepts of incomplete dominance, co-dominance, pleiotropy, epistasis, and polygenic traits support the erroneous concept of blending inheritance for they indicate that genes interact and have multiple phenotypic effects on organisms.

Color blindness is the most common genetic disorder, which affects almost one in every ten males. Color vision deficiency is a decreased ability to distinguish colors and, in some cases, may be an acquired disease. However, the majority of people have it as an inherited problem. In this condition, one or more of three cone cells in the eye fail to develop and are not able to distinguish color. Color blindness threatens male humans more frequently than female ones because the X chromosome mutation is the main reason for color blindness. Females have paired X chromosomes, and therefore, the first chromosome offsets the defect of the second.

Nevertheless, color blindness genes may be carried by the non-color-blind female and transferred to future generations (Bergendahl et al, 2019). Having a single X chromosome increases the risk for males as they will always have the genetic disease if the recessive gene is passed.

Inherited color blindness includes three different varieties: anomalous trichromacy, dichromacy and monochromacy. Two most prevalent forms of inherited color vision deficiencies are protanomaly and deuteranomaly, both of which are known as red-green color blindness and effect about 8% of human males and 0,6% of females (Seager et al., 2018). Depending on the mutation, inherited color blindness may be congenital or may reveal itself in childhood or adulthood.

The disease is not caused by a flaw in DNA transcription or translation as the parent chromosome already contains a deficiency which is transmitted to the child (Seager et al., 2018). Color vision deficiencies may be caused by deficient gene expression, which leads to an incorrect process of protein production, which, in turn, results in malformation of cone cells.

Question: Could you tell more about the process of genetically engineered substances production, such as human insulin?

References

Bergendahl, L. T., Gerasimavicius, L., Miles, J., Macdonald, L., Wells, J. N., Welburn, J. P., & Marsh, J. A. (2019). The role of protein complexes in human genetic disease. Protein Science, 28(8), 1400-1411. Web.

Seager, S. L., & Slabaugh, M. R., & Hansen, M. S. (2018). Chemistry for today: General, organic, and biochemistry (9^th ed.). Cengage Learning.

Introduction

Families at risk of developing genetic disorders are candidates for genetic counseling. These possible changes in gene structure might have adverse effects if not identified in time for family members and future generations (Biesecker et al., 2019). Genes form the basic structure of humans and are responsible for determining the specific character traits that make individuals unique. With approximately 24,000 genes in a body, there develops a risk for certain conditions and diseases when any of them mutates (Centers for Disease Control and Prevention, 2020). While a significant number of mutations have no health effects or contain positive attributes, a few can cause serious challenges including sickle cell disease and hemophilia (Pecker & Naik, 2018). Genetical counseling involves a number of steps to identify, test and educate individuals as shown in figure 1 below. Consequently, genetic counseling becomes crucial to identify such traits in individuals to allow adequate interventions or planning for their ultimate health effects.

Role of Genetic Counseling

Genetic counseling is essential in collecting the history and patterns to identify possible trends likely to cause inheritance. This develops the necessary data to calculate the chances of recurrence of certain genetic mutations in future generations (Mathiesen & Roy, 2018). Testing is done through comparison with normal DNA to identify potential defects as shown in figure 2 below. Aspects such as miscarriages and stillbirths in other family members can have an effect on a parent if they become inherited thus affecting the possibility of other pregnancies (Stevens, 2020). This therefore protects the health of a mother and provides alternatives during these initial stages of planning to raise a family.

Apart from that, genetic counseling can also provide information on possible health defects in the fetus during pregnancy. This is to identify any potential conditions in the baby that could affect them in infancy or early childhood as they grow and develop (Blesson & Cohen, 2020). Furthermore, any abnormal test results detected could identify possible problems in the mother that could affect the viability of the pregnancy (Reutter, 2021). Such counseling is recommended for all pregnant women to provide vital information that can assist in making decisions whether to terminate or proceed with the pregnancy especially in cases where extreme mutations likely to affect the infant’s life are detected.

Candidates for Genetic Counseling

Genetic counseling can be useful to individuals with family or close relatives who have confirmed genetic conditions. This can provide adequate family history that can determine the predisposition of an individual to inherit such a condition (Blesson & Cohen, 2020). Apart from that, parents with children diagnosed with genetic conditions can also use counseling to determine possible risks to future ones (Amendola et al., 2021). This is important to provide the parents with the necessary information that can advise their decisions on their planned future.

More so, pregnant women are also advised to undergo genetic counseling if they are above thirty-four years of age and have produced any form of abnormal screening during the prenatal stages (Perge & Igaz, 2019). Such mutations in genes are abnormal spots in DNA as shown in figure 3 below (Cirino et al., 2019). Further, women who have experienced miscarriages or stillbirths during earlier pregnancies are also great candidates for genetic counseling since they could be linked to genetic problems (Hoskovec & Stevens, 2018). This provides the opportunity to learn and identify problems based on their genes for future planning.

When Genetic Counseling is Recommended

Genetic counseling is important since it increases the knowledge of a family towards genetic conditions. In some cases, a family may have a history of misunderstood health problems that could have reoccurred across generations without proper medical diagnosis (LeRoy et al., 2020). In such cases, the benefits of such testing can be better explained to enable other family members to be tested and determine any other possible genetic problems.

Apart from that, counseling can help affected individuals to find the best psychosocial tools to assist with coping with any adverse results identified after testing. Counseling requires a trained individual who can talk humanely with a patient and discuss the outcomes as shown in figure 4. Therefore, finding the right methods to help in the transition to living with such conditions is important to prevent breakdowns that could further affect the family (Resta, 2019). Genetic counseling therefore forms a basis for future engagements that could be developed through the relationship between the counselor and family members.

Diseases Detected through Genetic Counseling

Ovarian, breast and colorectal cancer could be inherited by an individual if their family members were diagnosed with it. These types of cancers are caused by hereditary mutations in genes such as BRCA1 which can be passed on to other members of the family (Gardner et al., 2018). Apart from that, cystic fibrosis can also be detected through genetic screening. This condition is caused by gene mutations that result in difficulties in digestion and breathing especially in children due to mucus in the lung membranes as shown in figure 5 below (Zuckerman, 2021). Hemophilia, which is a disorder involving bleeding, can also be detected using genetics (Gardner et al., 2018). In such cases, affected individuals do not have the necessary functioning to assist with clotting.

Conclusion

Changes in gene structure might have adverse effects if not identified in time for family members. Therefore, genetic counseling becomes crucial to identify such genes in individuals to allow adequate interventions or planning for their ultimate health effects. This is useful to individuals with family, close relatives or children with confirmed genetic conditions and mothers who experienced miscarriage. Genetic counseling therefore increases the knowledge of a family towards genetic conditions and helps affected individuals to find the best psychosocial tools to assist with coping with outcomes.

References

Amendola, L. M., Golden-Grant, K., & Scollon, S. (2021). Scaling genetic counseling in the genomics era.Annual Review of Genomics and Human Genetics 22, 339-355. Web.

Arakelians, S. (2021). Pharmacy Clinical Pearl of the Day: Cystic Fibrosis.Pharmacy Times. Web.

Biesecker, B. B., Peters, K. F., & Resta, R. G. (2019). Advanced genetic counseling: Theory and practice. Oxford University Press.

Blesson, A., & Cohen, J. S. (2020). Genetic counseling in neurodevelopmental disorders.Cold Spring Harbor Perspectives in Medicine 10(4), Web.

Brooks, A. (2017). [Scientist holding a multi well plate used for genetic testing] [Stock image]. Alamy. Web.

Centers for Disease Control and Prevention. (2020). Genetic counseling. Centers for Disease Control and Prevention. Web.

Cirino, A. L., Seidman, C. E., & Ho, C. Y. (2019). Genetic testing and counseling for hypertrophic cardiomyopathy. Cardiology Clinics 37(1), 35-43. Web.

Gardner, R. J., Gardner, R. J., & Amor, D. J. (2018). Gardner and Sutherland’s chromosome abnormalities and genetic counseling. Oxford University Press.

Hoskovec, J. M., & Stevens, B. K. (2018). Genetic counseling overview for the obstetrician-gynecologist.Obstetrics and Gynecology Clinics of North America 45(1), 1–12. Web.

LeRoy, B. S., Veach, P. M., & Callanan, N. P. (2020). Genetic counseling practice: Advanced concepts and skills. John Wiley & Sons.

Lokare, S. (2022). [Image of DNA strand] [Stock image]. Unsplash. Web.

Mathiesen, A., & Roy, K. (2018). Foundations of perinatal genetic counseling. Oxford University Press.

Moharem-Elgamal, S., Sammut, E. & Stuart, G. (2020). Genetic counseling in inherited cardiomyopathies. Journal of the American College of Cardiology: Case Reports 2(3), 392-395.

Pecker, L. H., & Naik, R. P. (2018). The current state of sickle cell trait: Implications for reproductive and genetic counseling.Blood 132(22), 2331–2338. Web.

Perge, P., & Igaz, P. (2019). Family screening and genetic counseling. Experientia Supplementum 111, 29-32. Web.

Resta, G. R. (2019). What have we been trying to do and have we been any good at it? A history of measuring the success of genetic counseling.European Journal of Medical Genetics 62(5), 300-307. Web.

Reutter, M. H. (2021). Genetic counseling for birth defects. European Journal of Pediatric Surgery 31(6), 467. Web.

Stevens, B. (2020). Impact of emerging technologies in prenatal genetic counseling.Cold Spring Harbor Perspectives in Medicine 10(12). Web.

Zuckerman, S. (2021). The emergence of the “genetic counseling” profession as a counteraction to past eugenic concepts and practices. Bioethics 35(6), 528-539. Web.

Centers for Disease Control and Prevention. (2021). [An obstetrician consulting a pregnant patient] [Stock Image]. Unsplash. Web.

I believe that human genetic modification should be allowed. My main argument is that using genetic modification to improve the quality of human life is an effective use of scientific progress. Humanity can finally conquer such incurable diseases as cancer, aids, and cystic fibrosis through genetic engineering in medicine (Fernandes, 2021). This applies not only to adults but also to children. The modification of human embryonic DNA offers hope that gene mutations can be corrected and diseases prevented from being passed on (Blair, 2019). In the future, such procedures may result in children no longer being born with cystic fibrosis or with genes that increase the risk of cancer.

As for the genetic modification of animals and insects, it can also be beneficial. For example, thanks to CRISPR technology, modifying the gene responsible for carrying malaria in a mosquito could potentially eradicate the disease forever (Kahn, 2016). This is quite an encouraging statement, considering that many people, including children, are dying from malaria. However, this technology must have an apparent scope of application. The ecosystem of our planet is a fine-tuned mechanism in which all components are closely interconnected. Too much change or removal of one of them can have a catastrophic effect on the environment. Therefore, the genetic modification of animals and insects should be applied judiciously and carefully coordinated with environmental organizations.

In the case of humans, there must also be clear boundaries for modification. Genome adjustment for the purpose of curing a fatal disease or disability is entirely acceptable. However, this kind of intervention should be made only if other therapies are unsuccessful. In addition, I would not permit modification to change external parameters, such as eye color, hair color, or body shape. This technology should only be used in medical practice. Accordingly, only certified specialists in genetics and biology should have access to it. In addition, before being allowed to work with CRISPR, testing must be carried out to see whether the person is aware of what he or she is working with. In this way, genetic engineering will serve the good of humanity and cannot harm anyone.

References

Blair, A. (2019). Designer babies: Model status gene pools [Video]. TED. Web.

Fernandes, C. R. (2021).Eight diseases CRISPR technology could cure. Labiotech. Web.

Kahn, J. (2016). Gene editing can now change an entire species – forever [Video].TED. Web.

Significance of Research

Molecular biology is a huge subject with 30000 genes in mammalian genomes with 2 to the power of 30000 combinations of gene expressions (Soneji et al, 2007, p. 38). However, the possible gene expressions in real life are much less. Deep knowledge of architecture and the dynamic behavior of the transcription networks could reveal generation or reprogramming of cell fate for purposes of therapeutic or commercial benefit (Soneji et al, 2007, p. 38).

Development occurs when the ordered division of cells forms a whole organism. Signals and transcription factors that interact with one another to regulate the fate of individual cells control the process. These interactions, when viewed as a whole, form a genetic regulatory network. The regulation of development of cell behaviors like renewal, proliferation, differentiation, and death is not yet fully understood (Soneji et al, 2007, p. 31).

Cell-specific gene expression programs which are regulated by transcription factor interactions would help us to understand cell behaviors including development. Understanding the dynamics of genetic regulatory networks is an immense challenge to the future for the treatment of cancers, identifying congenital abnormalities, and the possibility of genetic engineering to cure or prevent them as required. The dynamics of these networks also throw light on the mechanisms of diseases that occur when the cellular processes are dysregulated. Accurate predictions can be made of the possibility of illnesses when these regulatory networks are affected (Karlebach and Shamir, 2008).

This research intends to explore ways to identify, model, test, and represent such networks to understand how transcription factors and signals work together to control development, and how cells are programmed to different phenotypes by using a variety of approaches, including in vivo, in vitro and in silico methods.

Review of Background of the Research

The School of Biology, Nottingham, is studying developmental genetics and gene control. Eukaryotic gene expression is focused upon in the research at this school. The embryonic development of vertebrates and the genetics involved is another focus. Mechanisms that regulate stem cell fate are mainly investigated in developmental studies (Loose, 2004). Stem cells from the nervous system, germ cells, and bone marrow-derived ones are being studied. Models are being developed by Dr. Matthew Loose for investigating how cell fate is controlled by the interplay of transcription factors and signals. The studies also include the control of transcription and the mechanisms of RNA maturation (Loose, 2004).

The modeling of genetic regulatory networks has evolved as the latest development in molecular biology. Global gene expression data sets and information of genome sequence from many species have made this possible through reverse genetic engineering (Soneji et al, 2007, p. 30). The hemopoietic stem cells are the most important of cells in the present era as they have unique biological properties which are of great interest to science, commercial purposes, and public interest. The molecular pathways are to be fully revealed.

The present information that has been accepted by researchers is that transcription factors are key regulators of cell activities (Enver and Greaves, 1998). It has been found that each cell has a different gene expression and cell fate is decided or changed by a change in a single transcription factor. However, cell combinations have varying gene expression patterns. The manners in which genes interact with each other provide a genetic regulatory network (Soneji et al, 2007, p.31). The decisions for the fate of the hemopoietic stem cell would be predicted by these networks.

Transcription factors and signals together have a functional relationship in the genetic regulatory network. The key determinants of cell fate are the transcription factors (Loose and Patient, 2004, p.467). Extracellular signals would trigger their binding with the DNA and gene transcription is regulated. Target genes would be other transcription factors and signals. This cross-regulation produces a relationship that would be stable when signals are not forthcoming. The molecular programming of cells during development would be provided by the extracellular signals, intracellular transcription factor responses, and the relationships between them (Loose and Patient, 2004, p. 467).

During embryonic development of the primary germ layers of ectoderm, mesoderm, and endoderm, part of the mesoderm and endoderm respond to inducing signals together and develop in a close relationship. This has been demonstrated in the amphibian Xenopus Laevis (Loose and Patient, 2004, p.467). Cardiac or other congenital abnormalities have also been attributed to defective development. The molecular pathways could be defective leading to this consequence. The highest abnormality seen at birth is a cardiac abnormality (McFadden, 2002).

A gene regulatory network has been developed for the specification of erythroid cells through the hemopoietic stem cell (Swiers, Patient and Loose, 2006). This network has a series of bipotential switches arranged in a cascade. It is believed that one pair of cross-antagonistic transcription factors could control two lineages in a mathematical model. This could be the pattern or motif seen throughout development (Loose and Patient, 2006). The transcription factors of GATA-1 and PU.1 mutually inhibit each other and model the process of lineage specification in hematopoietic cells (Roeder and Glauche, 2006). They create a situation that allows the progenitor cell to select between the erythroid megakaryocytic lineage and the myeloid-monocytic one. The transcription factors also promote the expression of genes that implement these lineages (Soneji et al, 2007, p. 37).

Computational methods have been developed with the help of microarray data sets to study the structure of the transcriptional networks from their dynamics. Several techniques have been adopted. The Probabilistic Boolean network has been found to be useful. High-quality data were obtained first from yeast. Mammalian stem cells are more difficult to handle for quality data as hematopoiesis is a complex system (Soneji et al, 2007, p. 35). The main issue would be to resolve cellular heterogeneity.

Specific Aims for Research

Genetic regulatory networks are being investigated to identify the networks by finding the transcription factors and the lineages. The model of linked networks is to be determined and the choice of fate made. The model would be tested for transcription –target gene relationship. The networks would be represented to understand how transcription factors and signals work together to regulate development. The promoters of the target would be having binding sites for the transcription factor which can either repress or activate (Loose and Patient, 2004, p. 468). The relationships would be classed directly if responding to the upstream factor when protein synthesis inhibitors are present. If there is no binding site, the relationship is indirect. Transcription factors that bind to the DNA through another transcription factor are also believed to be having a direct relationship. The intercellular signaling molecules are included in the research ((Loose and Patient, 2004, p. 468). The signaling molecules and transcription factors are to be labeled separately. The data obtained would be compared to the available statistics on the World Wide Web. The network is divided into time zones depending on the morphological and gene expression criteria. The various stages of development from fertilization onwards are followed carefully. The first stage could be up to the stage of mid-blastula and has the effects of the mother and the zygotic expression. Mid blastula transition has a surge of zygotic gene expression. Such a surge is again seen at a later stage or the late blastula stage (Loose and Patient, 2004, p. 468). The mesoderm and the endoderm are both well defined by the last stage.

Research approaches

A variety of approaches is employed. The in vivo approach would involve doing the study in live conditions. The in vitro approach would involve performing the research in laboratory conditions. The in silico approach is more effective for tracing the protein-protein interactions in the cells. Independent assessment procedures are possible using this approach. More data could be gathered too.

Researches on the development of cells have been done in the amphibian Xenopus Laevis. In vitro studies have been done on mouse haemangioblasts of the Mix+Brachyury+Flk-1+ (Swiers, 2007). Studies on the amphibian Ambystoma mexicanum (axolotl) show better results for germ cell specification than Xenopus. A cloned variety of axolotl homolog has shown only slight differences from the original variety (Swiers, 2007). Developmental studies have also been done on the sea-urchin. (Loose and Patient, 2004).

References

Enver, T. & M. Greaves. 1998. Loops, lineage, and leukemia. Cell 94: 9–12.

Karlebach, G. and Shamir, R. (2008). “Modelling and analysis of gene regulatory networks”. Nat. Rev. Mol Cell Biology, Vol. 9, No.10. Pg.770-780ю

Loose, M. and Patient, R. (2004). “A genetic regulatory network for Xenopus mesendoderm formation” Developmental Biology, Vol. 271, Pgs 467-478

McFadden DG, Olson EN. (2002). “Heart development: learning from mistakes”. Current Opinion Genetic Development 2002; 12:328–35.

Roeder, I. & I. Glauche. (2006). “Towards an understanding of lineage specification in hematopoietic stem cells: a mathematical model for the interaction of transcription factors GATA-1 and PU.1”. J. Theor. Biol.4: 852–865.

Soneji, S. et al. (2007). “Inference, Validation, and Dynamic Modeling of Transcription Networks in Multipotent Hematopoietic Cells”. Annals of New York Academic Science, Vol 1106, Pg 30-40, New York Academy of Sciences.

Swiers, G., Patient, R. and Loose, M. (2006). “Genetic regulatory networks programming haematopoietic stem cells and erythroid lineage specification”. Developmental Biology, Vol. 294, Pg 525-540, ScienceDirect, Elsevier.

Swiers, G. et al. (2007). “Exploring the role of Mix in mesoendoderm and blood specification in amphibians”, Program abstract 205, Institute of Genetics, University of Nottingham, Nottingham, UK.

What do they mean by “bad blood”?

In this particular case, bad blood refers to instances where a person has bad genes creating a greater likelihood that should they procreate with another individual, it is possible that their own children or even their children’s children will suffer from some form of genetic abnormality or disease. As seen in the case of the film “Bad Blood,” this fear manifests itself through varying forms of selective marriage practices as well as instances of distinct discrimination against individuals who have been identified as carriers of potentially unwanted genetic traits.

Why are people afraid of genetic diseases? What were the different ways that the people in the film respond to these fears of genetic mutations or diseases? What are the specific ways (biological and cultural) that they could overcome these fears?

The fear of genetic disease can be considered a manifestation of the inherent desire to have healthy children. All parents want what’s best for their children, and in this particular case, this desire became fear over what their children could possibly suffer if they had imperfect genes. It is actually a reasonable fear to have since the desire to procreate with a healthy and viable mate has been ingrained into us on a genetic level. It is also quite interesting to note that different individuals in the film had different responses to the fear of genetic disease. Some, such as those seen in the case of the people of Japan, seemingly attached a great deal of stigma to the issue of genetic “impurity,” resulting in few marriage prospects for those who were victims of the Hiroshima bomb.

On the other hand, others, such as the couple suffering from dwarfism, took to the issue of genetic mutations in a more accepting fashion. What is identifiable in all cases is that there is a great deal of social stigma attached to genetic mutations despite varying degrees of acceptance regarding certain genetic diseases or mutations. Taking this into consideration, the best way to allay such fears is to help people understand that the chances of passing on mutated genes are quite rare and will most unlikely never occur to them.

What is the take-home message of this film? What is the main argument of the film?

The take-home message that the film is trying to impart is the fact that though genetic mutations can be passed down from generation to generation, the fact remains that out of millions of cases, this can only happen once or twice. In other words, most individuals are quite safe from the possibility of acquiring a genetically recessive trait, and as such, we really shouldn’t put as much credence into genetic paranoia as we do today.

The main argument of the film relates to the issue of the people of Hiroshima and the possibility of their children possessing genetically mutated characteristics. The film states that based on the findings of various forays into the local population of Hiroshima, there was little evidence to suggest that the current population is at risk of creating a race of genetically mutated offspring, and as such, people should stop being obsessed over the issue of bad blood and just move on with their lives.

Why do you think modern genetic testing for diseases is important? What are the implications for quality of life for genetic testing? Consider what the increased risks of new biomedical knowledge are through genetic prescreening? What should we do with this new capability and knowledge?

From a certain perspective, it can be seen that testing for diseases is important since it helps parents be more aware of potential problems that may occur and take the necessary steps to be prepared for it. On the other hand, when it comes to introducing the possible social ramifications that commercialized genetic engineering could have on society, no example does it best than the movie “Gattaca.” In the film, we can see that instead of society being divided along with gender, ethnicity, or race, it has instead turned towards the quality of a person’s genetics as the primary means of determining an individual’s worth and place in society.

A person’s future is no longer dictated by the desire or ambition to make something of their life, but rather they are evaluated based on their genetic predispositions for intelligence, athleticism, or potential temperament in the workplace. In essence, a person’s future is, in effect, dictated not by fate, chance, ambition, desire, or intelligence but rather on the choices his/her parents had made before he/she was already conceived. One of the problems with genetic engineering is its potential to turn children into mere commodities with society ignoring the ethical ramifications of creating a generation of adults that had their lives planned since birth (The Case Against Perfection: Ethics in the Age of Genetic Engineering, 2007).

If a child’s future can be decided based on the types of genetic traits a doctor can include in his/her overall genetic makeup, parents could, in effect, decide whether their child will be a doctor, athlete, underwear model, or whatever career they desire. This, in effect, takes away a child’s choice to determine what their future will be and, in effect, turns them into a commodity rather than a unique individual with any number of potential futures ahead of them. In fact, it is based on this that it must be questioned whether this form of genetic “improvement” in effect takes a way a person’s freedom of choice.

It is everyone’s basic human right to have the freedom of choice, the freedom to choose their life, and as such, this is an indelible and irrevocable aspect of any person’s basic human rights. It is based on this that new knowledge into genetics should also come a certain degree of ethics and morality into the practice wherein we should not quantify the worth of an individual based on their genetic potential rather on what they themselves strive to achieve.

Through your own research, using the internet and library resources, identify and describe in detail another or different type of genetically inherited disease similar to the ones presented in the film (specifically one identified as Mendelian) that results from an autosomal dominant or recessive condition. Provide the name, and a brief summary of the mechanism of expression (genotype), location on the genome (if known), describe the onset, manner of manifestation, outcomes, population distribution, and if a particular behavioral or historical or environmental factor has been identified

Crohn’s disease is identified as a variation of the NOD2 gene and the protein attached to it; it is a genetically inherited defect classified as an inflammatory bowel disease (Raszewski, 2011). Overall manifestations of it come in the form of severe abdominal pain, vomiting, weight loss, skin rashes over certain parts of the body, constant fatigue, and inflammation of the eyes. To this day, Crohn’s diseases affect 48 out of every 100,000 individuals around the world and can manifest at nearly any age. There is currently no known cure; however, it isn’t considered particularly fatal due to certain forms of medication allowing the disease to enter into remission.

Reference List

Raszewski, R. 2011. Inflammatory Bowel Disease: The Essential Guide to Controlling Crohn’s Disease, Colitis and Other IBDs. Library Journal, 136 (19) – 90.

The Case Against Perfection: Ethics in the Age of Genetic Engineering. 2007. Publishers Weekly, 254 (11) – 51-52.

Reproduction is one of the most intricate and complex phenomena occurring in species, which is why examining it further will contribute tremendously to the understanding of cells development and the functioning of living organisms, in general. Mitosis is one of the two methods that are used on a cellular level for reproduction (Yanagida 3). Specifically, according to Yanagida, mitosis is “a morphological (cell structural) event, and a number of visible cell structural mitotic markers have been proposed, such as nuclear membrane disassembly, chromosome condensation, spindle formation, kinetochore microtubule formation, etc.” (p. 2).

By studying the concept of mitosis closer and understanding in greater detail what occurs on the cellular and molecular levels within cells during it, one will be able to approach a more accurate interpretation of the genetic makeup of different species.

The first step of mitosis can be described as the preparation for the following cell division. Mitosis starts with the stage known as prophase, which implies having chromosomes organized with the help of condensing (Saha and Begum 75). As a rule, at the specified stage of mitosis, cohesin contained in the sister chromasin arms is removed from the specified location so that individual sister chromatids could be successfully resolved (Li et al. 2596). Afterward, the preparation for the second stage of mitosis begins.

During the second phase, which is known as prometaphase, the actual cell division process is set into motion. Namely, at the moment of prometaphase, the nuclear envelope fragmentation occurs. Thus, the cell is split into tiny vessels that will serve as the building blocks for the daughter cells (Ikeda and Tanaka 1126). The specified stage of mitosis occurs at a particularly fast pace since it requires microtubules to assemble and dissipate when being produced in centrosomes (Zhang et al. 158).

Microtubules seek the opportunity to reattach as they undergo the process of assembling and disassembling, seeking kinetochores that can provide attachment sites to them (Ikeda and Tanaka 1127). Furthermore, as microtubules continue to grow, they stretch and expand the chromosomes, causing pole-directed forces to stabilize within the cells (Zhang et al. 159). As a result, when the prometaphase, chromosomes gain pole orientation (Ikeda and Tanaka 1127). The described change prepares the cells for the third stage of mitosis.

Next, a crucial change in the chromosomes of a cell occurs. During metaphase, which is the third stage of mitosis, chromosomes are arranged in the most compact manner possible (Guo et al. 1128). As the centromeres of a cell align among the spindle equator, the genetic material of the maternal cell is duplicated, which allows for the two daughter cells to emerge (Orr et al. 1086). When compared to the rest of the stages of mitosis, metaphase is, perhaps, the most peculiar one since it involves the process of splitting the genetic material into two identical sets (Orr et al. 1086). Partaking in a metaphorical tug of war, the kinetochores, or protein strands, allow for the duplication process to launch.

At the specified stage, the phenomenon known as the metaphase checkpoint occurs (Guo et al. 1128). The described stage is particularly important in the mitosis process since at the specified point in time, the cells that will divide are identified. Thus, as soon as all of the kinetochores are properly attached and aligned, the cells enter the fourth stage of the process.

The fourth phase of mitosis also deserves a separate description as a crucial part of the process. During the fourth phase, the cells that cells with properly aligned spindles enter the state of anaphase, during which sister chromatids are divided and set apart from each other. The process in question is known as anaphase and is set into motion as a result of the degradation of the cohesin molecules (Yanagida 2). The anaphase process leads to the production of two essential types of change, namely, the shortening of the kinetochore microtubules and their further motion toward the spindle poles (Wall et al. 3).

The fifth and the final stage of mitosis termed as the telophase implies the reformation of the membrane and the decondensation of the chromosomes. Finally, the cytokinesis ensues causing the eventual emergence of daughter cells (Li 2954). Ending with cytokinesis, namely, the process of cytoplasm being split to form two daughter cells, the specified stage ends with the emergence of two cells with identical genetic makeup (Abramo et al. 1395). Thus, mitosis ends, showing that replication of cells with the resulting production of two identical ones is a natural process within tissues in the human body, as well as in some organisms. Overall, observing mitosis helps to discover the intricate details of cell reproduction, thus, developing a clear idea of the genetic material transfer.

The exploration of the mitosis process is particularly useful from a biological perspective since it guides one’s understanding of the key changes occurring during it on biological and molecular levels, therefore, gaining a better idea of the genetic alterations within cells and the functions of specific chromosomes. Therefore, the phenomenon of mitosis is worth considering as an illustration of the changes within cells during the described reproduction method. With the understanding of mitosis, one will develop a clear idea of the key strategies of transferring genetic material from a maternal cell to the daughter cells.

Works Cited

Abramo, Kristin, et al. “A Chromosome Folding Intermediate at the Condensin-to-Cohesin Transition during Telophase.” Nature Cell Biology, vol. 21, no. 11, 2019, pp. 1393-1402.

Guo, Ao, et al. “Single-Cell Dynamic Analysis of Mitosis in Haploid Embryonic Stem Cells Shows the Prolonged Metaphase and Its Association with Self-Diploidization.” Stem Cell Reports, vol. 8, no. 5, 2017, pp. 1124-1134.

Ikeda, Masanori, and Kozo Tanaka. “Plk1 Bound to Bub1 Contributes to Spindle Assembly Checkpoint Activity During Mitosis.” Scientific Reports, vol. 7, no. 1, 2017, pp. 1-15.

Li, Xing, Fan Yang, and Boris Rubinsky. “A Theoretical Study on the Biophysical Mechanisms by Which Tumor Treating Fields Affect Tumor Cells during Mitosis.” IEEE Transactions on Biomedical Engineering, vol. 67, no. 9, 2020, pp. 2594-2602.

Orr, Bernardo, and Helder Maiato. “No Chromosome Left Behind: The Importance of Metaphase Alignment for Mitotic Fidelity.” The Journal of Cell Biology, vol. 218, no. 4, 2019, p. 1086.

Saha, Susmita, and Kazi Nahida Begum. “A Comparative Analysis on Mitotic Interphase and Prophase among Twelve Varieties of Brassica L. from Bangladesh: Brassicaceae.” International Journal of Biosciences, vol. 17, 2020, pp. 73-82.

Wall, Richard J., et al. “Plasmodium APC3 Mediates Chromosome Condensation and Cytokinesis during Atypical Mitosis in Male Gametogenesis.” Scientific Reports, vol. 8, no. 1, 2018, pp. 1-10.

Yanagida, Mitsuhiro. “The Role of Model Organisms in the History of Mitosis Research.” Cold Spring Harbor Perspectives in Biology, vol. 6, no. 9, 2014, pp. 1-15.

Zhang, Haoyue, et al. “Chromatin Structure Dynamics during the Mitosis-to-G1 Phase Transition.” Nature, vol. 576, no. 7785, 2019, pp. 158-162.

The issue of genetic testing is a highly controversial one, as its advantages and disadvantages present various dilemmas. It is still not clear if genetic testing should or should not become a common procedure that all people undergo regularly. I believe that it is an extremely personal decision to make. There are certain limitations and concerns that a diagnosed person can face, especially when they are diagnosed with untreatable and lethal disorders (Norrgard, 2008). Knowing about conditions like that may significantly decrease the quality of life and even lead to depression and anxiety.

At the same time, I acknowledge all the benefits that genetic testing can bring in terms of diagnosing a wide range of diseases and conditions. Fearing that they might discover hereditary predispositions to some untreatable diseases, many people choose not to get tested. However, I believe that deep inside, they still think about it and have concerns; I would if my family had a history of genetic conditions. That is why some people may even feel relieved when they undergo testing and have to face difficult results. At least they can know for sure that they are predisposed to certain conditions and focus on ways to improve their lives (Kurian et al., 2019). After all, genes are believed to be malleable; a positive approach, holistic nutritional program, and avoiding environmental toxins will not harm any person whose genetic testing results show a predisposition to certain diseases.

In the end, I do not think there is a universal answer to this question. Each person’s choice has to be authentic because they are the ones who will have to live their lives with this knowledge. I do believe, though, that scientific and health communities might focus more on raising awareness about genome sequencing, with particular reference to conditions that can be caught in the early stages, such as different types of cancer.

References

Kurian, A. W., Ward, K. C., Howlader, N., Deapen, D., Hamilton, A. S., Mariotto, A., Miller, D., Penberthy, L. S., & Katz, S. J. (2019). Genetic testing and results in a population-based cohort of breast cancer patients and ovarian cancer patients. Journal of Clinical Oncology, 37(15), 1305-1315.

Norrgard, K. (2008). Genetic testing and family planning | Learn science at Scitable. Scitable.

Criminality is influenced by diverse social factors and reflects social situation in a particular country. Also, critics and researchers underline that rates of criminality depends upon biological and genetic influences as drivers of antisocial behavior patterns. The relationship between biological and genetic characteristics and the life consequence of criminal behavior is observed for other events: life expectancy, mobility, automobile accidents, and suicide.

Biological influences on criminality are evident in sex differences between males and females. Sex of a person makes it possible to experience various life consequences. The belief that females, who are supposedly physically more weak, are mistreated more often is also inaccurate. Aside from rape, the only individual crime for which women are victimized more than men is robbery with contact. Men are twice as likely to be the victim of an assault or a robbery and 50 percent more likely to experience some crime of theft. Men are also the victims of strangers more than females. Some 72 percent of all personal crimes of violence against males involve strangers, compared with only 57 percent of the violent crimes against females. This connection holds for property crimes as well. Therefore, the idea that physically weaker people constantly fall prey to the criminal has no foundation in fact. Neither females nor older people are particularly prone to criminal victimization. On the contrary, they are considerably less likely to be victims than their counterparts. But, the lifestyles of these community groups may explain this fact better than their actual vulnerability to criminals (Wright et al 2008).

Human biology and genetics are the two personal attributes most closely tied to antisocial behavior. Heredity and race are also related. Contrary to what one might expect, the differences among groups are not dramatic. Blacks are more frequently victims of violence than others, while whites experience property crimes at higher rates than other ethnic and racial groups. For crimes of violence, robbery accounts for the higher rate experienced by blacks. Blacks are almost three times more likely than whites to be a robber’s victim. For property crimes, blacks are more vulnerable to purse-snatching and pocket-picking than whites, but whites experience higher rates of larceny without contact. This general pattern of oppression is consistent across ethnic lines. Individuals of Hispanic and African-American background are more prone to violent ill-treatment but less likely to suffer property crime than non-Hispanics (Beaver, 2008)

Genetic predisposition may lead to antisocial inclinations and increase a possibility of criminal behavior patterns. The cultural ties associated with family income, race, and ethnicity also affect with whom one associates and the places of those associations. Housing, transportation, privacy, and leisure-time factors are related to income as well as to racial and ethnic segregation. To the extent that crime varies according to place and event, individuals from different income levels and racial and ethnic groups will experience crime to varying degrees. The chances of criminal victimization appear to vary according to the time a person spends in public places, particularly at night, the proportion of time spent with non-offenders, and degree to which a person shares unique biological characteristics with offenders. The decrease in official statistics is accomplished by simply changing the techniques for recording complaints. When the same departments are faced with budget cuts and fierce competition for scarce resources with the fire department, sanitation workers, and other local agencies, indications that crime is increasing and law enforcement is imperative becomes socially advantageous (Wright et al 2008).

Researchers (Wright et al 2008) admit that the young, male, unmarried or divorced, and poor face higher risks of criminal victimization. According to researchers, individuals characterized by more than one of these variables have exceedingly high victimization rates. By biological age, individuals differ in mobility, exposure to others, and time spent outside the home. Very young children are not often exposed to criminal victimization because few activities involving that age-group occur outside the home. They are under the constant supervision and protection of an adult. This pattern begins to change when a young individual starts school. The individual spends greater amounts of time away from home with non-family members. With adulthood, lifestyle shifts again. Job and familial responsibilities buffer a person from antisocial environments. As one progresses through adulthood, mobility, interpersonal contacts, and the external world become more and more restricted. Fear of crime also increases with age, contributing to the further reduction in exposure to victimization as older adults avoid unsafe places (Beaver, 2008)

In sum, biology and genetic factors have a great impact on a person and his/her behavior patterns. Individuals from the antisocial families experience the highest rates of victimization for most crimes. Household larceny and motor vehicle thefts (where wealthy families are more likely to be victimized) are the two exceptions to this pattern. The biological factors lead to violent crime. This is true for all violent crimes except rape, where women from poor families are nine times more likely to be attacked than women from wealthy families. Another important difference among income categories is that poor individuals are much more likely to be seriously injured when robbed or assaulted than more affluent individuals. Still, genetic factors dominate among all social groups in spite of their income level.

References

Beaver, K.M. (2008). Biosocial Criminology: A Primer. Kendall/Hunt Publishing Co.; 1 edition.

Wright, J.P. Tibbetts, S.G. Daigle, L.E. (2008). Criminals in the making: Criminality across the life course, Sage Publications, Inc.