By using 16-F self-retaining feeding catheters, fluoroscopically guided percutaneous gastrostomy was performed in 68 consecutive adult patients without the use of gastric fixation devices. Short-term (2-week) follow-up of all patients was available, with 30-day follow-up obtained in 94% of the study group (n = 64). Thirty-day mortality was 12%, with no procedure-related deaths. Major and minor morbidity rates were 4.7% and 7.8%, respectively. The mean procedure time was 7 minutes. These data compared favorably with those of series employing smaller catheters placed with and without the use of gastropexy, as well as surgical gastrostomy and gastropexy procedures. Percutaneous placement of large-caliber (16-F) gastrostomy catheters is safe, effective, and rapid in the adult population and can be accomplished routinely without the use of prior gastropexy.
These studies describe induction of a delayed anovulatory syndrome (DAS) by estradiol (E2) in female C57BL/6J mice. Six days after birth, female mice were injected s.c. with 0.1 micrograms estradiol benzoate or oil. Over 90% of the oil-injected controls exhibited estrous cycles from 2 to 9 mo of age. In contrast, 60% of the E2-injected mice exhibited estrous cycles at 2 mo of age but were acyclic by 9 mo; these mice were considered to have exhibited a DAS, and had longer cycles than controls. At 12 mo, ovarian impairments were assessed by examining 1) ovulation after s.c. injection of 5 IU human chorionic gonadotropin (hCG), and 2) estrous cycles after grafting into young (3-mo-old) hosts. Simultaneously, neuroendocrine impairments were assessed by examining 1) the surge of luteinizing hormone (LH) induced by E2 implants after ovariectomy, and 2) estrous cycles after receiving ovarian grafts from 3-mo-old mice. Ovaries from DAS and control mice ovulated equally in response to hCG. Ovaries from DAS mice grafted into young ovariectomized hosts supported 30% more cycles, of shorter period, compared with ovaries from control donors. However, the E2-induced LH surge was 50% smaller in DAS mice than in controls. Ovariectomized DAS hosts with ovarian grafts from young mice supported 70% fewer estrous cycles, of longer period, compared with ovariectomized control hosts with young grafts. We conclude that the E2-induced DAS in female mice is not due to ovarian impairments, but seems to result from neuroendocrine impairments.
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