Ranney School

Sexual harassment is a pervasive problem that affects individuals in a variety of social contexts, especially in the workplace and public spaces. Researcher has examined the complex phenomenon of women's non-resistance to sexual harassment and explore in depth the psychological, sociocultural and reproductive factors that lead women to not actively oppose or confront sexual harassment. Drawing on both evolutionary and survival perspectives, the paper explores the complex interplay between reproductive strategies, survival motivations, and social norms. Through the survey-based approach, we qualify the relationship between the women's varying responses to sexual harassment and harasser's social-economic status and physical appearance, taking into account scenarios in the workplace, campus, and public spaces. The results showed that women's resistance to sexual harassment changed with the various degrees of social status and appearance of the harasser. The implications of this research extend to understanding gender dynamics, workplace policies, and the social impact of sexual harassment. The study also acknowledges the limitations of sample representation and cultural context, providing avenues for future research on this important and sensitive topic. By revealing the multifaceted nature of non-resistance, it helps to understand womens experiences and decisions more fully in the face of sexual harassment.

In this article, we shall prove the following two basic results of arithmetic dynamics. Let ƒ: P¹(<i>K</i>) → P¹(<i>K</i>) be a rational function of degree 𝑑 &gt; 1. Discovered during the research, there are different results shown with the different definitions of <i>K</i>. If <i>K</i> is an algebraically closed field of characteristic 0, then <i>#Fix</i>(ƒ^<i>n</i>) = 𝑑^<i>n</i> + <i>0</i>(1). If <i>K</i> is a number field, then there are only finitely many preperiodic points of ƒ.

Students participating in the Students Modeling A Research Topic (SMART) Team partnership program involving Henry E. Lackey High School, University of Maryland, Baltimore County, and Milwaukee School of Engineering used 3D printing technology to create a physical model of the soluble form of CD80 glycoprotein and researched its role in regulating proteins known to prevent T‐cell activation. The CD80 glycoprotein has two immunoglobulin‐like (Ig‐like) domains connected by an interdomain linker region. These Ig‐like domains bind to CD28, CTLA‐4 and programmed death ligand‐1 (PDL‐1) proteins. The expression of PDL‐1 on human cancer cells prevents tumor cells from T‐cell attack and elimination. In recent experiments, CD80 was shown to play a role in the cell surface expression of PDL‐1. Specifically, the transfection of the gene coding for CD80 into human cancer cells has inhibited expression of PDL‐1, the mechanism of which is unclear. Further exploration of soluble CD80 may improve understanding of its interactions with PDL‐1 and aid the development of a soluble CD80 immunotherapy for cancer. Supported by a grant from the HHMI Pre‐College Program School and NIH #RO1CA84232 to Ostrand‐Rosenberg.