A Statistical Study of Operating Systems at Harrisburg University

We conducted a survey of 100 students to find out which operating system students are using for their main school laptop. (Class Project

JAK2 Inhibition Impairs Proliferation and Sensitises Cervical Cancer Cells to Cisplatin-Induced Cell Death

Persistent infection with high-risk human papillomavirus (HPV) is the underlying cause of ~5% of all human cancers, including the majority of cervical carcinomas and many other ano-genital and oral cancers. A major challenge remains to identify key host targets of HPV and to reveal how they contribute to virus-mediated malignancy. The HPV E6 oncoprotein aberrantly activates the signal transducer and activator of transcription 3 (STAT3) transcription factor and this is achieved by a virus-driven increase in the levels of the pro-inflammatory cytokine interleukin-6 (IL-6) in HPV positive cervical cancers cells. Crucially, STAT3 activity is essential for the proliferation and survival of cervical cancer cells, suggesting that targeting STAT3 may have therapeutic potential. Unfortunately, the development of direct STAT3 inhibitors has been problematic in the clinic due to toxicity issues identified in early stage trials. To overcome this issue, we focused on the protein Janus kinase 2 (JAK2), which phosphorylates STAT3 and is essential for STAT3 activation. Here, we demonstrate that inhibiting JAK2 reduces cell proliferation and induces apoptosis in HPV transformed cervical cancer cells. We further establish that this is due to inhibition of phosphorylation of the JAK2 substrates STAT3 and STAT5. Finally, we demonstrate that the clinically available JAK2 inhibitor Ruxolitinib synergises with cisplatin in inducing apoptosis, highlighting JAK2 as a promising therapeutic target in HPV-driven cancers

Fibroma Causing Compartment Syndrome in NCAA Division I Athlete

Please enjoy Volume 6, Issue 1 of the JSMAHS. In this issue, you will find Professional, Graduate, and Undergraduate research abstracts, and case reports. Thank you for viewing this 6th Annual OATA Special Edition

The role of STAT3 during the human papillomavirus (HPV) life cycle and in HPV-associated cervical cancer

Human papillomaviruses (HPV) activate a number of host factors to control their differentiation-dependent life cycles. The manipulation of these host cell signalling pathways can result in the developement of cancer and HPV is responsible for around 5% of all cancers worldwide. Gaining a better understanding of these virus: host interactions is critical for the development of treatments for HPV infection and associated cancers. The transcription factor signal transducer and activator of transcription (STAT)-3 is important for cell cycle progression and cell survival in response to cytokines and growth factors. STAT3 requires phosphorylation on Ser727, in addition to phosphorylation on Tyr705 to be transcriptionally active. Although STAT3 has been shown to be hyperactive in many cancers, including cervical cancer, there is a paucity of information on the role of STAT3 during the productive HPV life cycle and HPV-associated cancers. Utilising a primary keratinocyte system to study the full HPV life cycle, this study demonstrates that STAT3 is essential for the HPV18 life cycle in both undifferentiated and differentiated keratinocytes. Furthermore, the HPV E6 oncoprotein is identified to be sufficient to induce the dual phosphorylation of STAT3 at Ser727 and Tyr705 by a mechanism requiring Janus kinases and members of the MAPK family. Importantly, silencing of STAT3 protein expression by siRNA or inhibition of STAT3 activation by small molecule inhibitors, or by expression of dominant negative STAT3 phosphorylation site mutants, results in blockade of cell cycle progression. Organotypic raft cultures of HPV18 containing keratinocytes expressing a phosphorylation site STAT3 mutant display a profound reduction in suprabasal hyperplasia, which correlates with a loss of cyclin B1 expression and increased differentiation. Finally, increased STAT3 expression and phosphorylation is observed in HPV positive cervical disease biopsies compared to normal cervical tissue, highlighting a role for STAT3 activation in cervical carcinogenesis. In confirmation of this, STAT3 phosphorylation was demonstrated to be in increased in HPV+ cervical cancer cells when compared to HPV- cervical cancer cells. Detailed mechanistic study identified that this was due to an increase in IL-6 auto/paracrine signalling induce by HPV E6 in an NFkB-dependent manner. Finally, STAT3 was demonstrated to essential for the proliferation, migration and invasion of HPV+ cervical cancer cells. Utilisation of a clinically available inhibitor of JAK2, an upstream kinase for STAT3, also resulted in a similar impairment of proliferation, migration and invasion. In summary, our data provides evidence of a critical role for STAT3 in the HPV18 life cycle and in HPV+ cervical cancer cells. This suggests a possible therapeutic target for both HPV infection and in the treatment HPV+ cervical cancer

Achilles Tendon Rupture in NCAA Division I Football Athlete

Please enjoy Volume 6, Issue 1 of the JSMAHS. In this issue, you will find Professional, Graduate, and Undergraduate research abstracts, and case reports. Thank you for viewing this 6th Annual OATA Special Edition

Tradeoffs in Community Properties Through Time in a Desert Rodent Community

Resource limitation represents an important constraint on ecological communities, which restricts the total abundance, biomass, and community energy flux a given community can support. However, the exact relationship among these three measures of biological activity remains unclear. Here we use a simple framework that links abundance and biomass with an energetic constraint. Under constant energetic availability, it is expected that changes in abundance and biomass can result from shifts in the distribution of individual masses. We test these predictions using long-term data from a desert rodent community. Total energy use for the community has not changed directionally for 25 years, but species composition has. As a result, the average body size has decreased by almost 50% and average abundance has doubled. These results lend support to the idea of resource limitation on desert rodent communities and demonstrate that systems are able to maintain community energy flux in the face of environmental change, through changes in composition and structure

Screening for Colon Cancer in Adults Under and Over 50: Effects on Mortality Rates

Recently, there has been an increase in the number of adults under the age of 50 who are diagnosed with colon cancer, and many of these adults are diagnosed with stage III or IV. In 2018, the recommended age for initial colon cancer screening through colonoscopies decreased from age 50 to 45. Despite this, there are rising concerns about the effectiveness of current screening mechanisms and the recommended age for screening. These authors pose the question: among adults under the age of 50, how does colon cancer screening impact mortality rates compared to those over the age of 50? A literature search was conducted using PubMed, CINAHL, and Nursing Reference Center Plus with the following search terms: colon cancer, screening, mortality, young adults. Requirements included that all articles be peer-reviewed and published in 2019-2024. A total of 12 articles met the inclusion criteria. The current evidence has shown that colonoscopies are effective in preventing colon cancer in adults aged 50 and older and have led to decreases in mortality rates for this group. Research suggests that routine screening in adults 45 and younger could also help to diagnose colon cancer at earlier stages and decrease mortality rates. Studies conducted outside the United States have shown that alternative screening methods, such as blood and fecal testing, are useful in screening young adults for colon cancer. Based on these findings, future recommendations include lowering the age requirement for colonoscopies and increasing accessibility to alternative screening methods

Intra-guild compensation regulatesspecies richness in desert rodents

Evidence from numerous studies suggests that species richness is an emergent property of local communities. The maintenance of species richness, despite changes in species composition and environmental conditions, requires compensatory colonization and extinction events with species coming from a regional pool. Using long-term data from a rodent community in the Chihuahuan Desert, we use randomization methods to test the null hypothesis that changes in species richness occur randomly. We find that the dynamics of species richness differ significantly from a random process, and that these nonrandom dynamics occur largely within the most speciose guild. Finally, we propose a general framework for assessing the importance of species compensation in maintaining biodiversity within local communities. Our results highlight the importance of niche complementarity and compensation in maintaining relatively constant species richness over time

Co-parenting: Taking the high road after divorce

The Oklahoma Cooperative Extension Service periodically issues revisions to its publications. The most current edition is made available. For access to an earlier edition, if available for this title, please contact the Oklahoma State University Library Archives by email at [email protected] or by phone at 405-744-6311