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spinal cord level. CS may explain the frequent coexistence of endometriosis with other conditions in the pelvis, such as painful bladder syndrome, irritable bowel syndrome, vulvar vestibulodynia, and myofascial pain conditions (9). Women with PPP also frequently experience psychological distress, catastrophising thoughts, kinesiophobia, and sleep disturbance. Although there is a growing understanding of the processes at play, there is still a paucity of evidence on how to best manage this challenging condition. It is our premise that improvement in pain, function, and quality of life can be better achieved if the peripheral nociceptive triggers, psychosocial factors, and central sensitivity are addressed concurrently. With this goal in mind, the BC Women's Centre for Pelvic Pain and Endometriosis was founded in 2011 to offer interdisciplinary management of PPP and to provide a platform for research in this area. Evaluation of the PPP/endometriosis patient Women with endometriosis and/or pelvic pain are referred to our centre by their family physician or specialist. We are a tertiary centre of care, with four gynaecologists evaluating approximately 1000 patients per year coming from the entire province of British Columbia (population of 4.7 million, spread out over 947,000 km 2) (10). Prior to their initial visit to the clinic, patients are required to complete extensive online questionnaires, which cover demographics, medical history, childhood sexual and physical abuse history, previous treatments, current severity of dysmenorrhea, non-menstrual pelvic pain, dyspareunia, and dyschezia (11). In addition, we use validated questionnaires to assess sleep (12), as well as to screen for irritable bowel syndrome (IBS) (13) and painful bladder syndrome (PBS) (14). Patients who score high on

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The purpose of this study was to compare the regional distribution of apoptotic cells in the near term ovine fetal brain caused by prolonged moderate hypoxia, as seen in placental insufficiency, and intermittent severe hypoxia, as seen in umbilical cord compression, which may then contribute to adverse neurodevelopment in the postnatal life. We hypothesized that apoptosis in the fetal brain will be increased in response to both prolonged moderate hypoxia and intermittent severe hypoxia. Twenty-one near term (126-127 days) sheep were divided into 3 groups: control (CON; n = 7), placental embolization (EMB; n = 7), and umbilical cord occlusion (UCO; n = 8). The EMB group had microsphere injections into the umbilical arterial circulation until the oxygen content was at 50% of baseline value. The UCO group had complete cord occlusion for 2 minutes every hour, 6 times a day for 2 consecutive days. At 4 pm on day 2, the animals were euthanized; fetal brains were fixed and prepared for apoptosis staining using the terminal uridine deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay method. In the cerebellar white matter, there was a 3-fold increase in the number of TUNEL positive cells per 1000 cells in both EMB and UCO animals as compared to CON (P = .017). There was also a significant increase in the frontal cortical grey matter (layers 1-3) in EMB animals as compared to CON (P = .014). As such, apoptosis in the near term fetal sheep brain is altered with both sustained moderate hypoxia and intermittent severe hypoxia in the latter part of pregnancy, with potential for long-term neurological sequelae.