Gynaecological care of women with chronic pelvic pain: Patient perspectives and care preferences.

OBJECTIVE: To explore the experiences and care preferences of women with chronic pelvic pain, with or without a history of sexual trauma, seeking gynaecological care. DESIGN: Qualitative study. SETTING: Ambulatory endometriosis centre. POPULATION OR SAMPLE: Women aged 18-55 years with chronic pelvic pain. METHODS: Baseline demographics and sexual trauma history were obtained, and participants were assigned to focus groups according to a positive (four groups, 13 participants) or negative (two groups, nine participants) screen for a history of sexual trauma. The focus groups were led by a clinical psychologist and a gynaecological surgeon and consisted of semi-structured interviews. The interviews were audio-recorded and transcribed, and the transcripts were coded in NVivo 12. MAIN OUTCOME MEASURES: Content analysis was used to derive themes according to the participants' own words. RESULTS: Participants with chronic pelvic pain, with or without a history of sexual trauma, experienced delay in diagnosis and repetitive dismissals by clinicians. Participants' experiences of dismissals included: clinicians not listening, insufficient allocation of time to appointments and perceived redundant medical testing (i.e. sexually transmitted infection testing, urine cultures, ultrasounds). Participants identified clinician interactions as pivotal in coping with both pelvic pain and sexual abuse. Participants also provided feedback regarding trauma-informed practices and care delivery specific to patients with chronic pelvic pain. CONCLUSION: Patients with chronic pelvic pain, with or without a history of sexual trauma, report negative experiences when interacting with the healthcare system. They have clear needs and preferences regarding gynaecological care and provide feasible suggestions for improving care delivery.

POPS case: A 30-year-old Filipino woman with fevers, lymphadenopathy, painful scalp lesions, and a neck mass.

We described a case of a 30-year-old Filipino woman who presented with fevers, night sweats, left hip pain, painful scalp lesions, and a neck mass. Symptoms began 6 months earlier, with nasal drainage, fever, cough, and occasional hemoptysis, which did not resolve with outpatient antibiotics. A further workup revealed lymphadenopathy and several lytic bone lesions. Her hospital course was later further complicated by the development of a tracheoesophageal fistula secondary to an esophageal mass and, then later, aseptic meningitis. Extensive diagnostic workup and immunologic tests were performed and finally led to the diagnosis. Here, we discussed the diagnostic workup and pathophysiology of the underlying condition. This case illustrated the importance of appropriate immunologic workup to make the diagnosis of a rare condition that proves to be clinically significant and presents challenges in management.

Brain glucose transporter (Glut3) haploinsufficiency does not impair mouse brain glucose uptake.

Mouse brain expresses three principal glucose transporters. Glut1 is an endothelial marker and is the principal glucose transporter of the blood-brain barrier. Glut3 and Glut6 are expressed in glial cells and neural cells. A mouse line with a null allele for Glut3 has been developed. The Glut3(-/-) genotype is intrauterine lethal by 7days post-coitis, but the heterozygous (Glut3(+/-)) littermate survives, exhibiting rapid post-natal weight gain, but no seizures or other behavioral aberrations. At 12weeks of age, brain uptake of tail vein-injected ((3))H-2-deoxy glucose in Glut3(+/-) mice was not different from Glut3(+/+) littermates, despite 50% less Glut3 protein expression in the brain. The brain uptake of injected ((18))F-2-fluoro-2-deoxy glucose was similarly not different from Glut3(+/-) littermates in the total amount, time course, or brain imaging in the Glut3(+/-) mice. Glut1 and Glut6 protein expressions evaluated by immunoblots were not affected by the diminished Glut3 expression in the Glut3(+/-) mice. We conclude that a 50% decrease in Glut3 is not limiting for the uptake of glucose into the mouse brain, since Glut3 haploinsufficiency does not impair brain glucose uptake or utilization.

Developing potent human uric acid transporter 1 (hURAT1) inhibitors.

The kidneys are a vital organ in the human body. They serve several purposes including homeostatic functions such as regulating extracellular fluid volume and maintaining acid-base and electrolyte balance and are essential regarding the excretion of metabolic waste. Furthermore, the kidneys play an important role in uric acid secretion/reabsorption. Abnormalities associated with kidney transporters have been associated with various diseases, such as gout. The current study utilized Xenopus oocytes expressing human uric acid transporter 1 (hURAT1; SLC22A12) as an in vitro method to investigate novel compounds and their ability to inhibit (14)C-uric acid uptake via hURAT1. We have prepared and tested a series of 2-ethyl-benzofuran compounds and probed the hURAT1 in vitro inhibitor structure-activity relationship. As compared to dimethoxy analogues, monophenols formed on the C ring showed the best in vitro inhibitory potential. Compounds with submicromolar (i.e., IC(50) < 1000 nM) inhibitors were prepared by brominating the corresponding phenols to produce compounds with potent uricosuric activity.