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Kim, Jury,Sapp, Harold L,Plummer, Caryn E,Brooks, Dennis E,Kim, Daeyoung,Kim, Min-Su The Society ; Maruzen Co. [distributor] 2012 The Journal of veterinary medical science Vol.74 No.10
<P>The objective of the study was to examine changes of intraocular pressure (IOP) undergoing anesthesia in Rhesus Macaques (Macaca mulatta) with Laser-induced Ocular Hypertension. Twenty male rhesus macaques (hypertensive glaucoma eye in OD; normal eye in OS) between 6 and 20 years of age were used for the study. The monkeys were anesthetized with ketamine hydrochloride (10 mg/kg intramuscularly) and 1% isoflurane, and then IOP in both eyes was measured by a single investigator using a calibrated Tonopen(TM) applanation tonometer (Mentor, Norwell, MA, U.S.A.). The mean IOP with ketamine anesthesia was 36.70 12.04 (right eye: OD) and 15.88 2.84 (left eye: OS). The mean IOP with isoflurane anesthesia was 19.98 6.67 (right eye: OD) and 15.32 2.15 (left eye: OS). Undergoing isoflurane anesthesia, the IOP of OD was significantly decreased. Conclusively, careful examination of IOP is required to prevent unexpected contraindication on glaucoma patient with isoflurane anesthesia.</P>
Peck, Jacquelin,Sapp, Kaitlin,Wilsey, Alexander,Wilsey, Michael The Korean Society of Pediatric Gastroenterology 2019 Pediatric gastroenterology, hepatology & nutrition Vol.22 No.1
Buried bumper syndrome is a rare but potentially severe complication of percutaneous endoscopic gastrostomy tube insertion. Though this complication is uncommon, it may lead to pressure necrosis, bleeding, perforation, peritonitis, sepsis, or death. Each case of buried bumper syndrome is unique in terms of patient comorbidities and anatomic positioning of the buried bumper. For this reason, many approaches have been described in the management of buried bumper syndrome. In this case report, we describe the case of an adolescent Caucasian female who developed buried bumper syndrome three years after undergoing percutaneous endoscopic gastrostomy insertion. We review diagnosis and management of buried bumper syndrome and describe a novel technique for bumper removal in which we use a guide wire in combination with external traction to maintain a patent gastrostomy lumen while removing the internal percutaneous endoscopic gastrostomy bumper.
Jacquelin Peck,Kaitlin Sapp,Alexander Wilsey,Michael Wilsey 대한소아소화기영양학회 2019 Pediatric gastroenterology, hepatology & nutrition Vol.22 No.1
Buried bumper syndrome is a rare but potentially severe complication of percutaneous endoscopic gastrostomy tube insertion. Though this complication is uncommon, it may lead to pressure necrosis, bleeding, perforation, peritonitis, sepsis, or death. Each case of buried bumper syndrome is unique in terms of patient comorbidities and anatomic positioning of the buried bumper. For this reason, many approaches have been described in the management of buried bumper syndrome. In this case report, we describe the case of an adolescent Caucasian female who developed buried bumper syndrome three years after undergoing percutaneous endoscopic gastrostomy insertion. We review diagnosis and management of buried bumper syndrome and describe a novel technique for bumper removal in which we use a guide wire in combination with external traction to maintain a patent gastrostomy lumen while removing the internal percutaneous endoscopic gastrostomy bumper.
Kim, Yun Joong,Yi, Yong,Sapp, Ellen,Wang, Yumei,Cuiffo, Ben,Kegel, Kimberly B.,Qin, Zheng-Hong,Aronin, Neil,DiFiglia, Marian 한림대학교 환경·생명과학연구소 2003 [일송 국제심포지엄] 노화와 만성퇴행성 신경질환 Vol.- No.5
The Huntington's disease (HD) mutation is a polyglutamine expansion in the N-terminal region of huntingtin (N-htt). How neurons die in HD is unclear. Mutant N-htt aggregates in neurons in the HD brain; expression of mutant N-htt in vitro causes cell death. Other in vitro studies show that proteolysis by caspase 3 could be important in regulating mutant N-htt function, but there has been no direct evidence for caspase 3-cleaved N-htt fragments in brain. Here, we show that M-htt fragments consistent with the size produced by caspase 3 cleavage in vitro are resident in the cortex, striatum. and cerebellum of normal and adult onset HD brain and are similar in size to the fragments seen after exogenous expression of human huntingtin in mouse clonal striatal neurons. HD brain extracts treated with active caspase 3 had increased levels of N-htt fragments. Compared with the full-length huntingtin, the caspase 3-cleaved N-htt fragments, especially the mutant fragment, preferentially segregated with the membrane fraction. partial proteolysis of the human caspase 3-cleaved N-htt fragment by calpain occurred in vitro and resulted in smaller N-terminal products: products of similar size appeared when mouse brain protein extracts were treated with calpain. Results support the idea that sequential proteolysis by caspase 3 and calpain may regulate huntingtin function at membranes and produce N-terminal mutant fragments that aggregate and cause cellular dysfunction in HD.