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排序方式: 共有371条查询结果,搜索用时 15 毫秒
81.
R W Hurst L J Bagley S Galetta G Glosser A P Lieberman J Trojanowski G Sinson M Stecker E Zager E C Raps E S Flamm 《AJNR. American journal of neuroradiology》1998,19(7):1267
PURPOSEDural arteriovenous fistulas (DAVFs) are acquired arteriovenous shunts located within the dura. The highly variable natural history and symptomatology of DAVFs range from subjective bruit to intracranial hemorrhage and are related to the lesion''s pattern of venous drainage and its effect on the drainage of adjacent brain. We examined the prevalence and features of DAVFs in patients with progressive dementia or encephalopathy.METHODSThe records and radiologic studies of 40 consecutive patients with DAVFs treated at our institution were reviewed.RESULTSFive (12.5%) of 40 consecutive patients with DAVFs had encephalopathy or dementia. In each patient, high flow through the arteriovenous shunt combined with venous outflow obstruction caused impairment of cerebral venous drainage. Hemodynamically, the result was widespread venous hypertension causing diffuse ischemia and progressive dysfunction of brain parenchyma. Results of CT or MR imaging revealed abnormalities in each patient, reflecting the impaired parenchymal venous drainage. Pathologic findings in one patient confirmed the mechanism of cerebral dysfunction as venous hypertension. The hemodynamic mechanism and resulting abnormality appeared identical to that seen in progressive chronic myelopathy resulting from a spinal DAVF (Foix-Alajouanine syndrome). Remission of cognitive symptoms occurred in each patient after embolization.CONCLUSIONVenous hypertensive encephalopathy resulting from a DAVF should be considered a potentially reversible cause of vascular dementia in patients with progressive cognitive deficits. 相似文献
82.
Zager P Nikolic J Raj DS Tzamaloukas A Campbell M 《Current opinion in nephrology and hypertension》2000,9(3):279-283
The prevalence of hypertension is extremely high in end-stage renal disease, and is a probable contributor to the epidemic of cardiovascular disease in end-stage renal disease. However, the paucity of prospective, randomized clinical trials makes it difficult to precisely define treatment strategies. Therefore, at present time the guidelines developed by the National Kidney Foundation's Cardiovascular Disease Task Force should be followed. 相似文献
83.
84.
Neuropeptides in human memory and learning processes 总被引:2,自引:0,他引:2
The neuropeptides vasopressin, adrenocorticotropin (ACTH), and beta-endorphin seem to have important effects on memory and learning. Animal studies attempting to demonstrate these effects are difficult to interpret because of the complexity of behavior that is described as "learning" and the impossibility of assessing verbal learning in animals. This article therefore reviews some of the animal literature on neuropeptides and learning, but focuses primarily upon studies in humans, both in normal volunteers and in patients with neurological disorders. Vasopressin enhances learning under some conditions. Intranasal administration has been associated with improvement on psychometric tests in patients with mild Alzheimer's disease and Korsakoff's psychosis, although these findings are not uniform. It improves performance on memory tests in normal volunteers, but does not seem to improve the memory deficit after head trauma. Cerebrospinal fluid levels are low in patients with Alzheimer's disease. ACTH and melanocyte-stimulating hormone (MSH) are two peptides the primary behavioral effect of which seems to be on attention or goal-motivated behavior rather than on memory processes themselves. Visual discrimination and the ability to continue repetitive tasks are enhanced; in mentally retarded subjects, the administration of ACTH or MSH improves performance on a variety of neuropsychological tests. It does not, however, improve cognitive function in the elderly. Endogenous opioids including beta-endorphin and met-enkephalin seem to have primarily an amnesic effect in animal studies. Their role in human learning is still uncertain, although naloxone, which antagonizes their effects, has been associated with improved cognitive performance in patients with Alzheimer's disease. These data underscore the complexity of the processes associated with human memory and the rudimentary state of our present knowledge. Whatever the mechanisms, however, vasopressin, ACTH, and endogenous opioids seem to have important effects upon memory. 相似文献
85.
Kristy K. Broman Tasha M. Hughes Lesly A. Dossett James Sun Michael J. Carr Dennis A. Kirichenko Avinash Sharma Edmund K. Bartlett Amanda AG. Nijhuis John F. Thompson Tina J. Hieken Lisa Kottschade Jennifer Downs David E. Gyorki Emma Stahlie Alexander van Akkooi David W. Ollila Jill Frank Jonathan S. Zager 《Journal of the American College of Surgeons》2021,232(4):424-431
86.
Zager JS Gusani NJ Derubertis BG Shaw JP Kaufman JP DeNoto G 《Journal of laparoendoscopic & advanced surgical techniques. Part A》2001,11(4):255-258
BACKGROUND: Crohn's disease confined to the appendix is rare but has been well described in the literature. It can mimic acute appendicitis clinically. After surgical treatment, recurrences of Crohn's disease are rare. We report the first case of treatment by laparoscopic appendectomy of Crohn's disease confined to the appendix. METHODS: A healthy 32-year old man presented with a week-long history of vague lower abdominal pain. Diagnostic work-up, which included CT, enteroclysis, and routine blood work, revealed a patent appendiceal lumen with an inflammatory mass in the right lower quadrant. RESULTS: Diagnostic laparoscopy revealed an inflamed appendix, and a laparoscopic appendectomy was performed, with frozen-section examination revealing Crohn's disease of the appendix. Two years after surgery, the patient has not had a recurrence of symptoms. CONCLUSIONS: Crohn's disease of the appendix can mimic acute appendicitis, although often with a more indolent course. The disease may be treated successfully by laparoscopic appendectomy, with good long-term results. 相似文献
87.
88.
Carr Michael J. Sun James DePalo Danielle Rothermel Luke D. Song Yun Straker Richard J. Baecher Kristin Louie Raphael J. Stahlie Emma H. A. Wright G. Paul Naqvi Syeda Mahrukh Hussnain Kim Youngchul Sarnaik Amod A. Karakousis Giorgos C. Lowe Michael C. Delman Keith A. van Akkooi Alexander C. J. Ollila David W. Collichio Frances Zager Jonathan S. 《Annals of surgical oncology》2022,29(2):791-801
Annals of Surgical Oncology - Talimogene laherparepvec (T-VEC) is an oncolytic virus approved for the treatment of unresectable, recurrent melanoma. The role of T-VEC after progression on systemic... 相似文献
89.
Carr Michael J. Sun James DePalo Danielle Rothermel Luke D. Song Yun Straker Richard J. Baecher Kristin Louie Raphael J. Stahlie Emma H. A. Wright G. Paul Naqvi Syeda Mahrukh Hussnain Kim Youngchul Sarnaik Amod A. Karakousis Giorgos C. Lowe Michael C. Delman Keith A. van Akkooi Alexander C. J. Ollila David W. Collichio Frances Zager Jonathan S. 《Annals of surgical oncology》2022,29(2):804-805
Annals of Surgical Oncology - 相似文献
90.
R A Zager 《Circulation research》1992,70(1):20-28
This study assessed gentamicin's effects on ischemia/reperfusion renal injury to better understand when and how it worsens postischemic acute renal failure. Rats were subjected to 25 minutes of renal pedicle occlusion with and without preischemic (15-minute) or postischemic (15-minute or 8-hour) gentamicin treatment (100 mg/kg, by itself a subtoxic dose). Gentamicin's impact on hypoxia/reoxygenation injury to isolated rat proximal tubular segments was also assessed. Preischemic and postischemic gentamicin worsened the severity of acute renal failure to the same degree, suggesting that pretreatment induces its effect in the reperfusion period. Gentamicin paradoxically lessened hypoxic damage to proximal tubular segments (assessed by lactate dehydrogenase release), again implying no adverse impact on oxygen deprivation-induced tubular injury. From 0-4 hours of reperfusion, gentamicin approximately halved ATP/ADP ratios (due to increased ADP), indicating a drug-induced defect in cellular energetics. This abnormality temporally correlated with evolving morphological damage. Although antioxidants (deferoxamine and sodium benzoate) have been reported to protect against pure aminoglycoside nephrotoxicity, they did not mitigate gentamicin's adverse impact on postischemic acute renal failure. Gentamicin did not influence ischemia/immediate reperfusion deacylation/reacylation (assessed by renal free fatty acid content) despite its known antiphospholipase activity. Although in the normal kidney gentamicin preferentially accumulated in cortex, in the postischemic kidney, both cortex and outer medullary stripe developed striking (approximately threefold to fivefold) and comparable gentamicin increments. In conclusion, gentamicin appears to exacerbate postischemic acute renal failure by adversely influencing the reperfusion, not the ischemic injury, process. This may occur because increased gentamicin accumulation negatively impacts on reperfusion cellular energetics. 相似文献