Bariatric surgery and endometrial pathology in asymptomatic morbidly obese women: a prospective, pilot study.

OBJECTIVE: To determine the prevalence of occult uterine pathology in asymptomatic, morbidly obese women before and after bariatric surgery-induced weight loss. DESIGN: Prospective, blinded, non-interventional cohort. SETTING: Urban teaching hospital. POPULATION: Morbidly obese women. METHODS: Endometrial biopsies were obtained at the time of Roux-en-Y gastric bypass and again 1 year later. Both the patient and the physician were blinded to the results of the initial biopsy until the conclusion of the study. Specimens were independently reviewed by two blinded pathologists. MAIN OUTCOME MEASURE: Effect of bariatric surgery-induced weight loss on the prevalence of endometrial pathology at 1 year. RESULTS: Fifty-nine women underwent an endometrial biopsy during bariatric surgery. The mean (range) age, weight, and body mass index (BMI) were 42 years (22-62 years), 127 kg (87-176 kg), and 46.8 kg/m(2) (36-64.3 kg/m(2) ), respectively. Four women had hyperplasia (three simple and one complex), for an overall prevalence of 6.8%. The prevalence among women not receiving some anti-estrogen therapy was 9.5%. Forty-six women (78%) underwent follow-up biopsy after a mean (range) weight loss of 42 kg (19-67 kg). Simple hyperplasia was identified in 3/46 women at the 1-year follow-up (6.5%). Two women had resolution of hyperplasia, two women had persistent, simple hyperplasia, and one had had a normal initial biopsy. No woman showed progressive pathology or cancer. At the end of the follow-up all but one patient had a documented resolution of endometrial pathology. CONCLUSIONS: Asymptomatic morbidly obese women are at relatively high risk of harbouring occult endometrial hyperplasia. Bariatric surgery-associated weight loss reduced but did not eliminate this risk for endometrial pathology.

AAV-P125A-endostatin and paclitaxel treatment increases endoreduplication in endothelial cells and inhibits metastasis of breast cancer.

Endostatin potentiates the antimitotic effects of paclitaxel (taxol) on endothelial cells (ECs). P125A-endostatin and taxol-treated ECs showed multipolar spindles and nuclear lobulation, leading to mitotic catastrophe and cell death. Induction of nuclear abnormalities was found to be dependent on ß-catenin levels as wnt-mediated overexpression of ß-catenin reversed the changes in nuclear morphology. These results prompted us to investigate whether antiangiogenic gene therapy and paclitaxel chemotherapy can synergistically inhibit angiogenesis and tumor growth. We first determined the effect of combination treatment in a transgenic mouse model of breast cancer. Intramuscular injection of recombinant adeno-associated virus type-2 virus induced sustained expression of P125A-endostatin. In vivo studies showed that combination therapy inhibited mammary cancer growth, delayed the onset of multifocal mammary adenocarcinomas, decreased tumor angiogenesis and increased survival in treated mice. In a second model, female athymic mice were orthotopically transplanted with a metastatic human breast cancer cell line. Antiangiogenic gene therapy in combination with paclitaxel inhibited tumor angiogenesis and lung/lymph-node metastasis in this model. These studies demonstrate cooperation between endostatin gene therapy and chemotherapy to inhibit tumor initiation, growth and metastasis.

Association between nonbacterial thrombotic endocarditis and hypoxigenic pulmonary diseases.

Observation of patients with nonbacterial thrombotic endocarditis (NBTE) in the setting of hypoxia from various lung diseases raised the question of a possible pathogenetic relationship between hypoxia and the development of NBTE. We reviewed 50 autopsied patients with NBTE and compared them with 50 age/race/gender-matched control patients without NBTE. We noted the lung weight and graded the histopathological severity of lung involvement by disease, clinical respiratory compromise, and the extent of any cancer present. Patients with NBTE had heavier lungs (P < 0.01) and histologically and clinically more severe pulmonary disease (both P < 0.005). There was no statistically significant difference in the extent of metastatic cancer between the NBTE patients and the controls (P > 0.5). When patients with cancer were excluded from the group of NBTE cases, there was still a statistically significant preponderance in the mean lung injury and clinical compromise scores of the NBTE patients (both P < 0.05), but the difference in lung weight was no longer statistically significant (P > 0.05). The study suggests that, in some patients, hypoxia may lead to NBTE, possibly through altered coagulation states.

Fatal infection after a bee sting.

Life-threatening or even fatal bee infections can rarely develop after bee stings.