Does ovarian suspension during laparoscopic surgery for endometriosis reduce postoperative adhesions? A randomised controlled trial

In this thesis, I have explored complex pathology of endometriosis, described current management strategies and highlighted the common problem of postoperative pelvic adhesions, often associated with the surgical treatment of this condition. Intra-operative suspension of the ovaries to the anterior abdominal wall is a simple method used to facilitate ovarian retraction during surgery. We found in an observational (pilot) study that the prevalence of ovarian adhesions for each ovary was 56.3% after laparoscopic surgery for severe pelvic endometriosis. A prospective double-blind cross-over comparison randomised controlled trial (RCT) was completed to assess the effect of temporary ovarian suspension following laparoscopic surgery for severe pelvic endometriosis on the prevalence of postoperative ovarian adhesions. Suitable women were randomised to unilateral ovarian suspension for 36 to 48 hours in the postoperative period. A transvaginal ultrasound scan was performed three months after surgery to assess for the prevalence of ovarian adhesions. Our RCT concluded that there was no significant difference (P = 0.23) in the prevalence of postoperative ovarian adhesions between the suspended (20/52) and unsuspended (27/52) side (38.5 versus 51.9%) [odds ratio 0.56 (95% confidence interval 0.22–1.35)]. Using the ovarian suspension RCT as a basis, I have described the detailed journey of an RCT from its conception, protocol design, pilot study, trial management, analysis to publication of results. The rationale for our study design and methodology was discussed. Statistical considerations were made from the outset, which led to a pilot study. Issues surrounding the implementation of our trial including ethical approval, recruitment, consent, randomisation and details of data management were outlined. Finally, statistical analysis, conclusions, limitations and suggestions for future research were made. Current Controlled Trials: ISRCTN2424221

Natural history of ovarian endometrioma in pregnancy.

Ovarian endometriomas are classified as benign ovarian lesions. During pregnancy endometriomas may undergo major morphological changes which are referred to as 'decidualisation'. Decidualised ovarian endometrioma may resemble malignant ovarian tumours on ultrasound examination. The aim was to study variations in the morphology and size of ovarian endometriomas diagnosed on ultrasound during pregnancy

Chronic adiponectin deficiency leads to Alzheimer’s disease-like cognitive impairments and pathologies through AMPK inactivation and cerebral insulin resistance in aged mice

BACKGROUND: Insulin resistance is the major pathogenesis underlying type 2 diabetes mellitus (T2DM) and these patients have doubled risk of Alzheimer's disease (AD). Increasing evidence suggests that insulin resistance plays an important role in AD pathogenesis, possibly due to abnormal GSK3β activation, causing intra- and extracellular amyloid-beta (Aβ) accumulation. Adiponectin (APN) is an adipokine with insulin-sensitizing and anti-inflammatory effects. Reduced circulatory APN level is associated with insulin resistance and T2DM. The role of APN in AD has not been elucidated. In this study, we aim to examine if adiponectin deficiency would lead to cerebral insulin resistance, cognitive decline and Alzheimer's-like pathology in mice. METHODS: To study the role of adiponectin in cognitive functions, we employed adiponectin-knockout (APN-KO) mice and demonstrated chronic APN deficiency in their CNS. Behavioral tests were performed to study the cognitions of male APN-KO mice. Brains and tissue lysates were collected to study the pathophysiological and molecular changes in the brain of APN-KO mice. SH-SY5Y neuroblastoma cell line was used to study the molecular mechanism upon APN and insulin treatment. RESULTS: Aged APN-deficient mice displayed spatial memory and learning impairments, fear-conditioned memory deficit as well as anxiety. These mice also developed AD pathologies including increased cerebral Aβ42 level, Aβ deposition, hyperphosphorylated Tau proteins, microgliosis and astrogliosis with increased cerebral IL-1β and TNFα levels that associated with increased neuronal apoptosis and reduced synaptic proteins levels, suggesting APN deficiency may lead to neuronal and synaptic loss in the brain. AD pathologies-associated APN-KO mice displayed attenuated AMPK phosphorylation and impaired insulin signaling including decreased Akt induction and increased GSK3β activation in the hippocampus and frontal cortex. Aged APN-KO mice developed hippocampal insulin resistance with reduced pAkt induction upon intracerebral insulin injection. Consistently, APN treatment in SH-SY5Y cells with insulin resistance and overexpressing Aβ induce higher pAkt levels through AdipoR1 upon insulin treatment whereas the induction was blocked by compound C, indicating APN can enhance neuronal insulin sensitivity through AMPK activation. CONCLUSION: Our results indicated that chronic APN deficiency inactivated AMPK causing insulin desensitization and elicited AD-like pathogenesis in aged mice which also developed significant cognitive impairments and psychiatric symptoms.published_or_final_versio

Expectant management of ultrasonically diagnosed ovarian dermoid cysts: is it possible to predict outcome?

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