Table of Contents Economic Policy Causes and Consequences of the Subprime Crisis Brendan Dowling 11

There are also many examples of strictly feminine psychiatric disorders that bear a social stigma similar to that of hysteria and neurasthenia. Recently, there has been an interest in the possible disturbances that premenstrual syndrome and other psychiatric disorders like it can cause to a woman’s ability to make sounds decisions. In his book, Corrections: A Critical Approach, Michael Welsh discusses the relation between PMS and ideas about female incompetency: “Strong social resistance against women’s search for equality still persists, and one of the primary mechanisms used to offset the upward mobility of women in society is to question their competence.”⁹⁹ Just as hysteria was used in the nineteenth century to oppress women and prevent their social movement, so disorders such as PMS and post-partum depression are used to promote ideas about the incompetency of women to rise in social and political positions today. Welsh goes on to argue that this questioning of women’s competency in relation to feminine psychiatric disorders is a societal mechanism used to ostracize women, and that even jokes made about the disorders also demotes women: “Furthermore, sexist humor about PMS reflects deep-seated anxieties about women in positions of political power.”¹⁰⁰ This is particularly relevant as women are running for president in this upcoming election; many of their opponents reference feminine psychiatric disorders such as PMS as a reason why women should not be president. The term “anxiety” that Welsh uses surmises the reason why feminine nervous disorders still continue to be stigmatized: men are afraid of women usurping positions of power.

As has been proven again and again throughout this paper, hysteria and neurasthenia are socially constructed diseases designed to marginalize women. So then why study the history of these diseases if they are not rooted in any valid medical origins? The history of a disease that is not really a disease is essentially a study of a social movement – in this case, part of a history of the marginalization of a group. It is important to recognize the ways in which women were marginalized in American history, so that we may recognize the ways in which they continue to be marginalized. Illnesses such as PMS and post-partum depression have, in a way, replaced hysteria and neurasthenia as examples of culturally produced mental illnesses that oppress and alienate women. By studying these diseases in juxtaposition with the treatment of hysteria and neurasthenia in the nineteenth century, one can begin to move towards removing the social stigma surrounding feminine mental disorders, and simultaneously, the stigma surrounding mental disorders in general that pervades modern day American culture.

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364-71. Accessed November 17, 2015. http://www.jstor.org/stable/3404057.
Dodd, Jenifer. "'The name game': Feminist protests of the DSM and diagnostic labels in the

1980s." History of Psychology 18, no. 3 (August 2015): 312-23. Accessed November 17, 2015. http://dx.doi.org.ezproxy.trincoll.edu/10.1037/a0039520.

Sander L. Gilman, Helen King, Roy Porter, G. S. Rousseau, and Elaine Showalter, 3-65. Berkeley, CA: University of California Press, 1993. eBook.

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Massachusetts General Hospital; with remarks on Freud's method of treatment by 'Psycho-analysis.'" Journal of Abnormal Psychology 1, no. 1 (April 1906): 26-41. Accessed December 9, 2015. http://web.a.ebscohost.com.ezproxy.trincoll.edu/ehost/detail/detail?vid=3&sid=68273d90-1f93-40e4-aa13-1ec068119ae2%40sessionmgr4003&hid=4101&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#AN=1926-00765-001&db=pdh.

Gilman, Helen King, Roy Porter, G. S. Rousseau, and Elaine Showalter, 286-336. Berkeley, CA: University of California Press, 1993. eBook.

America." Social Research 39, no. 4 (Winter 1972): 652-78. Accessed November 17, 2015. http://www.jstor.org/stable/40970115.

Accessed December 9, 2015. http://www.apa.org/monitor/2012/01/go-rest.aspx.

Hysteria In The History Of Mental Health." Clinical Practice and Epidemiology in Mental Health 8 (October 19, 2012): 110-19. Accessed November 23, 2015. doi:10.2174/1745017901208010110.

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Accessed December 9, 2015. JSTOR.

Jordan Reid

Gene flow occurs in bacteria, as in all other organisms, such that DNA is transcribed into RNA which is then translated into proteins. It is through this unidirectional flow of genetic information that that organisms are able to construct proteins that help them to carry out life processes. However, organisms’ need for certain proteins is dependent upon different environmental factors that the organism itself has no control over. Therefore, the activity of the genes that code for such proteins must be regulated. This regulation of gene expression occurs at three different levels in the cell: Transcriptional, Translational, and Post-translational (Willey).

Accordingly, at the transcriptional level, regulatory proteins often work to control the rate of the transcription of DNA into RNA (Willey 2014). Translation, however, is most often regulated by blocking initiation (Willey 2014). Finally, post-translational regulation is carried out through the use of molecules which bind to proteins that have already formed (Willey 2014). These proteins work to alter the function of the proteins that have already been formed in order to better suit the environmental conditions at a given instance (Willey 2014 ).

Various environmental stimuli can trigger this regulatory response and many different types of pathways mediate the response. In the case of Serratia marcescens, temperature is seen to have an effect on gene expression that is clearly visual to a casual observer. At certain temperatures, Serratia marcescens produces the cell surface pigment prodigiosin. This surface pigment makes Serratia marcescens bacterial growth on a nutrient agar plate appear red. However, according to Williams no other function is currently being attributed to prodigiosin (1973). The pigment is thought to be a byproduct of other biosynthetic pathways and, perhaps, to be a secondary metabolite (Williams 1973). While secondary metabolites are not necessary for survival in any capacity, the absence of these metabolites can negatively effect an organism (Williams 1973).

In this study, one half of two separate nutrient agar plates were inoculated with Serratia marcescens. These plates were then grown at two different temperatures: room temperature and 37˚C, the temperature in the incubator. After 24 hours the plates were observed before other half of plate that was left at room temperature was then inoculated again with Serratia marcescens and placed into the incubator. The plate in the incubator was also inoculated again with Serratia marcescens after 24 hours, but it was placed at room temperature. Observations were once again made of the color of the bacterial growth on either side of either plate. The observations of the colors at different temperatures were used in order to draw conclusions about how the expression of the gene for the cell surface pigment prodigiosin is regulated in Serratia marcescens and to propose a possible mechanism by which this occurs.
Purpose

This study was conducted in order to determine the manner in which Serratia marcescens regulates the expression of the cell surface pigment prodigiosin. Based on observations of the production of prodigiosin by Serratia marcescens cultures at different temperatures, this study aimed to propose a possible mechanism by which Serratia marcescens regulates the gene that controls the production of prodigiosin.

2 Nutrient Agar Plates

Inoculation Loop

Procedure

Two nutrient agar plates were obtained and labeled as shown below using a marker to draw the line depicted on either plate.

Using aseptic technique, section A of the plate labeled #1 was then inoculated with Serratia marcescens growing on a nutrient agar plate using an inoculation loop. Section C of the plate labeled #1 was also inoculated with Serratia marcescens growing on a nutrient agar plate using an inoculation loop and aseptic technique. The plate labeled #1 was left at room temperature and the plate labeled #2 was placed in the incubator at 37˚C. After 24 hours, the plates were observed and compared to each other. Section B of plate #1 and section D of plate #2 were then inoculated with Serratia marcescens using an inoculation loop and aseptic technique. The plate labeled #1 was placed in the incubator at 37˚C and the plate labeled #2 was left at room temperature. After 24 hours, the plates were observed and compared to each other. These observations from each day were recorded used in order to propose a mechanism by which Serratia marcescens regulates the gene that controls prodigiosin production.

The results show that the bacteria grown at room temperature (plate 1, side A) is red in color. When transferred to the 37˚C incubator, however, the red color darkens at the center of the bacterial growth and that the bacterial growth is white around the edges of the growth. By day 2 hours the bacterial growth is also visibly denser on side A of plate 1. The bacteria grown at 37˚C on plate 1 (side B) is white in the center, but slightly pink around the edges of the bacterial growth. This bacteria is also smeared across a larger area than was the bacteria on side A.

On plate 2, the results show that bacteria grown at 37˚C (side C) is white in color with very few pink spots around the edges of bacterial growth. When this bacteria is transferred to room temperature, however, it remains white at the center of bacterial growth and becomes red around its edges. The bacteria grown at room temperature on plate 2 (side D) produces very little red pigment. The pigment is smeared throughout the bacterial growth and is not limited to the edges. This bacteria is also smeared across a larger area than was the bacteria on side D.

Table 1: Plate #1

	Day 1 (Room Temperature)	Day 2 (Incubator - 37˚C)
Photo
Description of Color	A All bacterial growth is uniformly bright red	A Red color has darkened slightly. Entirely white around the edges of the bacterial growth. Bacterial growth has grown somewhat more dense
		B Bacterial growth is white. Some pink regions around the edges of the bacterial growth. Bacteria spread out on a somewhat larger surface area than it was before

	Day 1 (Incubator - 37˚C)	Day 2 (Room Temperature)
Photo
Description of Color	C All bacterial growth is uniformly white with very few pink regions around the edges	C White at the center of bacterial growth, red around the edges
		D Bacterial growth is very faintly red with certain regions being more red than others in random spaces on the plate. Bacteria spread out on a somewhat larger surface area than it was before

Based on the observations obtained from this study, it may be concluded that Serratia marcescens grown at room temperature produces the pigment prodogiosin optimally. This conclusion is supported by the very saturated red color that is visible throughout the bacterial growth in section A of plate #1 on day 1 of this study (Table 1, Page 3). The observations obtained from this study also suggest that S. marcescens grown at 37˚C does not produce the pigment prodogiosin optimally. This conclusion is supported by the bacterial growth in section C of plate #2 on day 1 of this study (Table 2, Page 4). This bacterial growth appears to be white at its center and very sparingly pink around its edges (Table 2, Page 4).

The results of this study may also be used in order to support the conclusion that S. marcescens that is transferred from room temperature to an environment of 37˚C will stop prodogiosin production. This deduction is supported by the observation that the bacterial growth in section A of plate #1 on day 2 became white around its edges after being stored in the 37˚C for a 24 hour period (Table 1, Page 3). The loss of the red color that entirely saturated the bacterial growth on section A of plate #1 is indicative of the S. marcescens ceasing prodigiosin production (Table 1, Page 3; Table 2, Page 4). Similarly, the saturated red pigment that formed a thick ring around the edges of the bacterial growth on section C of plate #2 on day two suggests that S. marcescens that is transferred from an environment of 37˚C to an environment at room temperature will commence prodigiosin production (Table 2, Page 4). This may be concluded because this bacteria was predominantly white after 24 hours in the incubator at 37˚C, turned a prominent shade of red around the edges after 24 hours at room temperature.

The results also indicate that the red pigment, or prodigiosin is always present in cells. Even at 37˚C when the temperature is above optimal for prodigiosin production the red pigment is still present in small amounts as is indicated by the sparse red and pink pigment visible on plates stored at 37˚C (Table 1, Page 3; Table 2, Page 4). This suggests that the gene which controls prodigiosin production is always on, but is inhibited to some degree at higher temperatures. This inhibition results in the suboptimal production of prodigiosin which, in turn, results in the sparse pink and red pigment which borders the bacterial lawn grown at 37˚C (Table 1, Page 3; Table 2, Page 4).

It is for this reason that the type of regulation of gene expression that S. marcescens seems to use to control the gene responsible for prodogiosin production seems to be negative transcriptional control (Willey 328). Negative transcriptional control is one way in which gene expression is controlled at the transcriptional level. Negative transcriptional control is mediated by regulatory proteins called repressor proteins (Willey 328). These proteins bind to DNA to prevent the initiation of transcription (Willey 328). However, the disappearance of the prodigiosin that is seen on section A of plate #1 on day 2 suggests that some post translational regulatory mechanism may be involved as well. While it is possible that prodogiosin simply degrades quickly if it is not being produced at high enough levels, this is a subject that could be explored in further studies.

It is important to note that both on section A of plate #1 and on section C of plate #2 that the change in temperature was seen to effect the edges of the bacterial lawn of growth first (Table 1, Page 3; Table 2, Page 4). This phenomenon could be due to the fact that bacterial cells on the edge of a lawn of bacterial growth are most sensitive to temperature change in the environment surrounding them. It is also possible that this pattern is related to the manner in which the bacterial cells send out the signal to commence or cease the production of prodigiosin. However, further observations would be necessary before any conclusions were made regarding this observation. It is however, presumed that given more time all of the bacteria on section A of plate #1 would turn white so long as it was left at room temperature. Similarly, it is presumed that all of the bacteria on section C of plate #2 would turn red so long as it was left in the incubator at 37˚C.

In addition to this, the results from section A of plate # 1 suggest that quorem sensing plays some role in the production of prodigiosin in S. marcescens. From day 1 to day 2, the density of the lawn of S. marcescens had increased significantly (Table 1, Page 3). The cells in the center of this bacterial lawn, which are presumed to have not yet received the signal for the inhibition of the gene responsible for prodigiosin production, grew darker over the course of that 24 hour period (Table 1, Page 3). This suggests that more prodigiosin was being produced in these cells residing in the center of the bacterial lawn of growth. This direct relationship between the increased cell density and the increased production of prodigiosin visible in the results of this study suggests that whether or not S. marcescens cells produce prodigiosin and how much prodigiosin is produced is controlled by the S. marcescens cell population density.

Finally, the results from section B of plate #1 support the conclusions mentioned above. The conclusion that S. marcescens grown at 37˚C does not produce the pigment prodogiosin optimally is supported by the predominantly white color present on the bacterial growth (Table 1, Page 3). The conclusion that the gene which controls prodigiosin production is always on, but is inhibited to some degree at higher temperatures which results in suboptimal production of prodigiosin is also supported by the presence of some pink pigment on the bacterial growth (Table 1, Page 3).

The results from section D on plate #2 however, are slightly more troubling. While the red pigment that is indicative of prodigiosin is certainly present, the pigment is much less prominent and less saturated than that which is seen on section A of plate #1 on day 1 (Table 1, Page 3; Table 2, Page 4). In addition to this, the red pigment here is not limited to the center or to edges of the lawn of the S.marcescens growth, but rather distributed throughout the plate (Table 2, Page 4). These results seem incongruous with the results from the other plate sections which uniformly indicate that prodigiosin is produced optimally at room temperature, that prodigiosin is inhibited at higher temperatures, and that prodigiosin production begins and ceases first at the edges of the bacterial growth.

This abnormality could be related to residual warmth on the plate when it was inoculated with S.marcescens which could have caused the idiosyncratic prodigiosin production patterns observed. Alternatively, the fact the S. marcescens grown on section D on plate #2 at room temperature was grown next to section C which is presumed to have been producing a prodigiosin gene inhibitor could have effected prodigiosin production on section D since no physical barrier existed between the plates and the inhibitor could have travelled across the plate. Finally, this abnormality could be related to quorem sensing. The S. marcescens growth on section C is seen to be much more condensed in one area than is the growth on section D; This simply due to a slight difference in streaking technique (Table 2, Page 3). Since the growth on section D is more spread out, the red coloring is more sparse because bacterial cells are less concentrated in a given area making quorem sensing more difficult for the cells and thusly preventing the cells from producing more prodigiosin.