No description available.

OBJECTIVE: Premature ovarian failure is a disease with many far reaching and serious consequences. Little is known about the complete etiology of the disease or what women may be at an increased risk for developing it. We sought to evaluate the prevalence of premature ovarian failure among women born in the United States and women not born in the United States who were patients of Boston Medical Center. We compared the prevalence of POF in these two groups to evaluate any relationships that may exist between birthplace and premature ovarian failure. METHODS: We collected data from the data warehouse of Boston Medical Center. We used data from women who had an FSH test done between the ages of 18 and 40 before June 30, 2013 as the control. We also compiled data of women who had an FSH level over 15mIU/ml as well as those who had diagnoses in SDK and Logician. Birthplaces data was also compiled for those women who had an FSH level>15mIU/ml. RESULTS: Women born outside of the U.S had a slightly higher prevalence of POF when compared to women born in the United States. Data analysis showed a significant difference among the two groups with p<0.0001 for each group. When birthplace data was compiled, Haiti had the highest number of women with FSH>15mIU/ml with Cape Verde and the Dominican Republic having the next highest amounts of women. CONCLUSION: Our study highlights the possible relationship that exists between premature ovarian failure and birthplace. This was a preliminary study to gather data that may be used in future, more specific studies to be done on the topic. These future studies should further investigate the reason this relationship exists, other causes that may be associated with premature ovarian failure, and further analysis of the prevalence of POF in various areas of the world.

The treatment of most cancers can still be considered inadequate despite the steady progress being made. A prime example of this issue is with epithelial ovarian cancers; this disease presents a significant issue, with a 5-year survival rate of 46% and a survival rate of 28% in patients that develop metastatic disease. Since ovarian cancer has such a high mortality rate, effective treatment modalities are necessary to prolong the quality of life after diagnosis. Psychosocial stress is related to the progression, proliferation, and migration in cancer patients, but the mechanisms of this relationship are not fully understood. The present in vitro study investigated the ability of oxytocin, a neuropeptide associated with social support, to attenuate the stress response. Catecholamines, a subclass of stress hormones, were used to simulate the stress induced inflammation process in ovarian cancer cells. To evaluate oxytocin’s capacity to attenuate the stress response, the ovarian cancer cell lines SKOV3, HEYA8, OVCAR8, and OV432 were separately treated with the presence or absence of catecholamines with the addition of oxytocin. Protein expression of the oxytocin receptor was investigated using a western blot protocol. Oxytocin receptor, oxytocin, and IL-6 mRNA expression was evaluated by quantitative PCR. Treatment with Oxytocin attenuated the inflammatory response resulting from catecholamine treatment. The oxytocin receptor gene and protein were present in each cell line, suggesting that oxytocin has an anti-inflammatory role in the tumor microenvironment in ovarian cancer patients. These results provide a mechanism by which social support, working through the release of oxytocin, promotes an anti-inflammatory process in ovarian cancer patients. This study may shed light into new pharmacological approaches for the treatment of ovarian cancer.

No description available.

No description available.

No description available.

Acute aerobic exercise alters neurotrophic and growth factor concentrations, increases neural activity and improves cognitive and motor function. Additionally, acute exercise increases excitation and reduces inhibition in the motor cortex as assessed via transcranial magnetic stimulation (TMS). The propensity for exercise-induced neuroplasticity may be greater in females, as females show greater neuroplasticity induction following non-invasive brain stimulation (NIBS) compared to males. In females, NIBS yields greater neuroplasticity during ovulation, when estradiol levels are higher, compared to menstruation, suggesting that ovarian hormones may also impact exercise-induced neuroplasticity. To date, it is unknown whether biological sex and ovarian hormones impact neuroplasticity induced by acute aerobic exercise. The present thesis investigated the effects of biological sex and ovarian hormones on the magnitude and direction of neuroplasticity induced by acute aerobic exercise. Fourteen females and fourteen age- and fitness-matched males participated in two sessions in which dependent measures were acquired before and following a single bout of aerobic exercise. Females were tested in the follicular (~day 7) and luteal (~day 21) phases of the menstrual cycle and males were also tested on two occasions separated by ~14 days. The exercise intervention consisted of 5 minutes of warm up, 20 minutes of moderate intensity continuous cycling at 65-70% maximal heart rate, and 5 minutes cool down. TMS was used to obtain motor evoked potential (MEP) recruitment curves and short interval intracortical inhibition (SICI) from the right first dorsal interosseous muscle. Blood measures of estradiol, progesterone, testosterone, and brain-derived neurotrophic factor were assessed before exercise on both testing sessions. Results indicated that only females showed increases in MEP recruitment curve following exercise, and this occurred regardless of menstrual cycle phase. SICI did not change following exercise for males or females on either testing session. The estrogen to progesterone ratio in females was greater in the follicular phase compared to the luteal phase. There was a trend towards greater serum BDNF levels in females in the luteal phase compared to the follicular phase. Sex hormones and BDNF levels did not vary across sessions in males. These findings indicate biological sex, but not ovarian hormones, is an important factor to consider when inducing neuroplasticity using acute exercise. / Thesis / Master of Science (MSc)

Ovarian cancer is considered to be one of the deadliest gynecological diseases. Over 21,000 women are expected to be diagnosed with this fatal disease in 2020 alone. Obesity, but more specifically a high waist-to-hip ratio, is indicative of abdominal obesity and has been correlated with increased risk of ovarian cancer. How abdominal obesity contributes to this increased risk has not been clearly delineated but much of the current research has been focused on the role of adipocytes. However, in addition to the adipocytes, abdominal white adipose tissue contains the stromal vascular fraction (SVF) which includes stem and progenitor cell populations, immune cells, and fibroblasts. Since the SVF can also be recruited by the cancer cells, we investigated how obesity affects the survival and metastatic potential of cancer cells by investigating changes in the expression of genes that contribute to survival, proliferation, migration, adherence, and invasion. We used culture conditions that mimic the non-permissive peritoneal environment. Cancer related genes, such as Dkc1, Ccnd2, Lig4, and Snai2, were upregulated when adipose derived stem cells (ADSC) were added into MOSE-LTICv spheroids. It was found that peritoneal serous fluid (PSF) from obese mice significantly increased migration of MOSE-LTICv (Serum vs PSF, 517.8 vs 1158.6). These studies brought new knowledge into the field of obesity and ovarian cancer risk and provided direction for future studies involving potential cellular and molecular targets for ovarian cancer diagnosis and treatment. / Master of Science / Ovarian cancer affects many women in the United States. Obesity or more specifically, carrying more weight around the waist, can affect a woman's risk of developing ovarian cancer. Abdominal fat needs to be researched to see if abdominal obesity can affect ovarian cancer on the cellular level. Researchers have looked into how fat cells, known as adipocytes, can affect the progression of ovarian cancer, but more research needs to be done on the contributions of other cells found within adipose tissue. Other cells in abdominal fat include cells such as immune cells, stem and progenitor cells and fibroblasts. We have explored how adipose stem cells from obese mice affect the DNA or "the blueprints" of the cells, survival, and progression of mouse ovarian cancer cells. We found that when adipose stem cells are combined with ovarian cancer cells the expression of certain genes or particular "blueprints" increased. The genes whose expression increased included Dkc1, Ccnd2, Lig4, and Snai2 and when deregulated can cause ovarian cancer cells to become more aggressive. The abdominal fluid from obese mice was found to increase migration of ovarian cancer cells which simulates an increase in metastatic potential. This information has given new insight into the obesity and ovarian cancer relationship.

Obesity is a major global health concern due to its steadily increasing rates and significant contribution to numerous diseases, including cancer. Ovarian cancer specifically, is associated with a 30% increased risk with obesity, although the mechanisms for this are unknown. Waist-to-hip ratio has been especially associated with ovarian cancer, suggesting that visceral fat may be the greatest contributor. Here, we investigated individual visceral fat depots as independent contributors to cancer progression, specifically focusing on adipose tissue-derived stem and progenitor cells, which have previously been shown to be recruited by cancer cells and participate in cancer progression. We confirmed that ovarian cancer tumor burden was indeed significantly increased in mice on a high fat as compared to low fat diet. To further investigate mechanisms, we examined changes in progenitor populations that occurred in intra-abdominal parametrial (pmWAT), retroperitoneal (rpWAT), and omental (omWAT) white adipose tissue (WAT) depots with cancer presence. The greatest tumor burden was evident in omWAT, which also displayed an increase in CD45- cells but a decrease in adipose progenitor cells (APC) and endothelial progenitor cells, suggesting that there was an increase in stromal cells, but that the stem cells were pushed towards differentiation. PmWAT and rpWAT showed remarkably stable progenitor populations. However, a tumor from pmWAT had a significant presence of CD45- cells, actually matching that of its surrounding tissue and differing from the omWAT tumors, indicating that microenvironment has a major influence on tumor stromal cells. We also found that with high fat diet, many cancer-associated changes were exacerbated, such as an increased inflammatory response in all tissues and further decreases in APCs in omWAT. In vitro studies further confirmed that ovarian cancer cells and SVF cells were able to directly interact. Additionally, SVF cells were able to increase the proliferation, mobility, and invasiveness of cancer cells. Conversely, co-culturing also enhanced the proliferation and mobility of SVF cells, providing further evidence that SVF cells may be recruited by cancer cells and that their relationship may be bilateral. Thus, this study provides a good foundation for examining the cellular contributions of adipose tissue to cancer. By further characterizing the mechanism for the association between obesity and cancer development, we could find novel targets to decrease the progress of cancer development in at-risk obese individuals. / Ph. D.

Approximately 21,550 women were diagnosed with Ovarian Cancer (OVCA) in 2009 and 14,600 died from their disease, making it the number one killer of women among gynecological cancers. Seventy percent of cases of OVCA are not detected until the disease has progressed to stage III or stage IV. Both diagnosis and aggressive treatments for late-stage OVCA can have a negative impact on women's psychosocial well-being resulting in anxiety, depression, and fear. The purpose of this integrative review of literature was to evaluate interventions designed to improve psychosocial well-being in women with OVCA. This review of literature was conducted using the CINAHL, PsycINFO, and MEDLINE databases using various key terms including "ovarian cancer or neoplasm" and "psychological and psychosocial", "well-being", "fear or anxiety or depression". Five studies met the inclusion criteria and were included in this review. These interventions include psychosocial, psychoeducational, and personal counseling interventions. The findings indicate that these interventions result in a significant improvement in participant's psychosocial well-being including decreased depressive symptoms, fear, and anxiety. This evidence supports that there is a need for psychosocial intervention in women with OVCA. It also suggests that women with OVCA benefit from tailored interventions and one-on-one educational and counseling sessions. Clinicians can use this information to anticipate potential problems in their client's psychosocial well-being and provide more education and support or refer them for counseling. More research is needed about reducing the psychosocial sequelae that results in women with OVCA.