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Brandon Davis Jun Tang Li Zhang Dezhi Mu Xiangning Jiang Valerie Biran Zinaida Vexler Donna M. Ferriero 《International journal of developmental neuroscience》2010
The blood–brain barrier (BBB) plays an important role in the pathophysiology of central nervous system (CNS) disorders such as stroke and hypoxic–ischemic brain injury. Vascular endothelial growth factor (VEGF) is involved in angiogenesis and vasogenic edema during stroke and hypoxia. However, the role of VEGF in BBB permeability after hypoxia has not been fully elucidated. We therefore investigated VEGF effects in an in vitro BBB model using rbcec4 endothelial cell line with the stimulation of VEGF or hypoxia. In this study, BBB permeability was studied using 14C-sucrose detection. The expression of BBB tight junction protein ZO-1, and the expression and phosphorylation of vasodilator stimulated phosphoprotein (VASP), VEGF and VEGF receptor 2 (VEGFR2) were determined using fluorescent immunocytochemistry and western blot analyses. We found that hypoxia upregulated VEGF expression, and VEGF increased BBB permeability. Hypoxia also increased VASP phosphorylation, which was mediated, in part, through VEGFR2. We also found that VASP at tight junctions was co-localized with ZO-1 in cell–cell contacts. Our findings show that VASP phosphorylation is affected by hypoxia and VEGFR2 inhibition suggesting a role for VASP in BBB permeability. 相似文献
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Higgins RD Raju T Edwards AD Azzopardi DV Bose CL Clark RH Ferriero DM Guillet R Gunn AJ Hagberg H Hirtz D Inder TE Jacobs SE Jenkins D Juul S Laptook AR Lucey JF Maze M Palmer C Papile L Pfister RH Robertson NJ Rutherford M Shankaran S Silverstein FS Soll RF Thoresen M Walsh WF;Eunice Kennedy Shriver National Institute of Child Health Human Development Hypothermia Workshop Speakers Moderators 《The Journal of pediatrics》2011,159(5):851-858
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Acute hypoxia-ischemia results in hydrogen peroxide accumulation in neonatal but not adult mouse brain 总被引:4,自引:0,他引:4
The neonatal brain responds differently to hypoxic-ischemic injury and may be more vulnerable than the mature brain due to a greater susceptibility to oxidative stress. As a measure of oxidative stress, the immature brain should accumulate more hydrogen peroxide (H2O2) than the mature brain after a similar hypoxic-ischemic insult. To test this hypothesis, H2O2 accumulation was measured in postnatal day 7 (P7, neonatal) and P42 (adult) CD1 mouse brain regionally after inducing HI by carotid ligation followed by systemic hypoxia. H2O2 accumulation was quantified at 2, 12, 24, and 120 h after HI using the aminotriazole (AT)-mediated inhibition of catalase spectrophotometric method. Histologic injury was determined by an established scoring system, and infarction volume was determined. P7 and P42 animals were subjected to different durations of hypoxia to create a similar degree of brain injury. Despite similar injury, significantly less H2O2 accumulated in P42 mouse cortex compared with P7 at 2, 12, and 24 h after HI. In addition, less H2O2 accumulated in P42 mouse hippocampus compared with P7 hippocampus at 2 h. Since immature neurons are more vulnerable to the toxic effects of H2O2 than mature neurons, this increased accumulation in the immature brain may explain why the neonatal brain may be more devastated, even after a milder degree of acute hypoxic-ischemic injury. 相似文献
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Giuseppe Simone Leonardo Misuraca Umberto Anceschi Francesco Minisola Mariaconsiglia Ferriero Salvatore Guaglianone Gabriele Tuderti Michele Gallucci 《European urology》2019,75(3):492-497
Background
With the increasing adoption of novel technologies and anatomical techniques, surgical management of benign prostatic hyperplasia (BPH) provides significant benefits in terms of obstruction relief, early urethral catheter removal, and faster return to daily activities. However, the main pitfall of BPH surgery in sexually active men remains ejaculatory dysfunction (EjD), which permanently affects quality of life.Objective
To detail a novel technique for marking the intraprostatic urethra through a retrograde injection of indocyanine green to enhance selective dissection of prostatic lobes during urethra-sparing robot-assisted simple prostatectomy (US-RASP) with the use of near-infrared fluorescence imaging (NIFI).Design, setting, and participants
Between January and September 2017, 12 consecutive male patients, who had BPH, were sexually active, and were motivated to preserve ejaculatory function, underwent US-RASP.Surgical procedure
US-RASP with NIFI to enhance the identification and preservation of the prostatic urethra.Measurements
Clinical data were prospectively collected in our institutional RASP dataset. Perioperative and functional outcomes of US-RASP were both graded, and assessed according to Clavien grading system and validated questionnaires postoperatively (International Prostate Symptom Score [IPSS]; Male Sexual Health Questionnaire on EjD [MSHQ-EjD] Short Form) at 3 and 12 mo.Results and limitations
Median preoperative prostate size was 102 cc (interquartile range [IQR] 88–115). Median operative time was 150 min (IQR 145–170). Median estimated blood loss was 250 (IQR 200–350). Continuous bladder irrigation was avoided in 83.4% of patients. Median time to catheter removal was 7 d (IQR 7–7) with a median hospital stay of 3 d (IQR 2–3). At 1-yr follow-up, median IPSS score, International Index of Erectile Function score, and MSHQ-EjD Short Form score were 5 (IQR 4–8), 26 (IQR 26–28), and 12 (IQR 1–14), respectively. Satisfactory anterograde ejaculation was reported in eight patients (66%).Conclusions
We described a novel NIFI-guided technique to perform US-RASP. This technique showed promising early functional results, suggesting a significant role of intraprostatic urethral integrity for the preservation of ejaculatory function.Patient summary
We developed a novel robotic technique to perform simple prostatectomy with integral preservation of the prostatic urethra. This technique provided a high rate of ejaculatory function preservation. 相似文献57.
Presentation of type I Chiari malformation after head trauma 总被引:1,自引:0,他引:1
An unusual case of Type I Chiari malformation that became symptomatic after closed head injury is reported. The patient manifested transient upper extremity weakness, persistent lower cranial nerve dysfunction, and cerebellar signs that slowly resolved. Magnetic resonance images showed tonsillar ectopia but no displacement of the brain stem or syringomyelia. Type I Chiari malformation should be included in the differential diagnosis of patients who present with upper extremity weakness, lower cranial nerve palsies, or cerebellar signs after trauma. 相似文献
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Cerebral palsy: MR findings in 40 patients. 总被引:20,自引:0,他引:20
C L Truwit A J Barkovich T K Koch D M Ferriero 《AJNR. American journal of neuroradiology》1992,13(1):67-78
PURPOSE: We used MR to retrospectively analyze the brains of patients suffering from cerebral palsy, our aim being to determine MR's role in the assessment of brain damage and the relationship of pre-, peri-, and post-natal events to cerebral palsy. METHODS: Forty patients (aged 1 month to 41 years) underwent MR scanning and findings were correlated with clinical histories in all cases. RESULTS: Review of MR scans of 11 patients who had been born prematurely revealed findings of periventricular white matter damage, indicative of hypoxic-ischemic brain injury (82%), the chronology of which was difficult to determine. Among 29 patients who had been born at term, three major patterns emerged: (1), gyral anomalies, suggestive of polymicrogyria, consistent with mid-second trimester injury; (2), isolated periventricular leukomalacia reflecting late second- or early third-trimester injury; and (3), watershed cortical or deep gray nuclear damage, consistent with late third-trimester, perinatal or postnatal injury. In 16 (55%) of 29 patients born at term, MR findings of intrauterine brain damage were observed; in over half of these cases MR revealed developmental anomalies, which is nearly twice the rate reported in prior studies employing CT. CONCLUSIONS: Our results support a growing consensus that cerebral palsy in term infants is often the result of prenatal factors, and less commonly related to the perinatal period. 相似文献
59.
Protecting Neurons 总被引:5,自引:0,他引:5
Donna M. Ferriero 《Epilepsia》2005,46(S7):45-51
Summary: Brain injury evolves over time, often taking days or even weeks to fully develop. It is a dynamic process that involves immediate oxidative stress and excitotoxicity followed by inflammation and preprogrammed cell death. This article presents a brief overview of mechanisms of neuroprotection in the developing brain. Although the focus is on ischemic injury, the conclusions drawn apply to any type of brain insult—epileptic seizures, trauma, or ischemia.
Strategies of neuroprotection include salvaging neurons through the use of targeted pharmacotherapies, protecting neurons through preconditioning, and repairing neurons by enhancing neurogenesis. Drug therapies that dampen the impact of immediate and downstream postinjury events are only modestly effective in protecting the brain from ischemic injury. In experimental models, complete or true protection can be achieved only through preconditioning, a process during which an animal develops tolerance to an otherwise lethal stressor. Although of no clinical use, preconditioning models have provided valuable insight into how repair systems work in the brain. Cumulative evidence indicates that the same genes that are upregulated during preconditioning, those mediating true protection, are also upregulated during injury and repair. Specifically, hypoxic preconditioning and hypoxic-ischemic insult have been shown to induce hypoxia inducible factor-1 (HIF-1) and its target survival genes, vascular endothelial growth factor (VEGF), and erythropoietin (Epo) in rodents. Of particular interest is the upregulation of Epo, a growth factor that may have therapeutic potential in the treatment of ischemic stroke. At this time, however, the postinjury enhancement of neurogenesis appears to offer the best hope for long-lasting functional recovery following brain injury. 相似文献
Strategies of neuroprotection include salvaging neurons through the use of targeted pharmacotherapies, protecting neurons through preconditioning, and repairing neurons by enhancing neurogenesis. Drug therapies that dampen the impact of immediate and downstream postinjury events are only modestly effective in protecting the brain from ischemic injury. In experimental models, complete or true protection can be achieved only through preconditioning, a process during which an animal develops tolerance to an otherwise lethal stressor. Although of no clinical use, preconditioning models have provided valuable insight into how repair systems work in the brain. Cumulative evidence indicates that the same genes that are upregulated during preconditioning, those mediating true protection, are also upregulated during injury and repair. Specifically, hypoxic preconditioning and hypoxic-ischemic insult have been shown to induce hypoxia inducible factor-1 (HIF-1) and its target survival genes, vascular endothelial growth factor (VEGF), and erythropoietin (Epo) in rodents. Of particular interest is the upregulation of Epo, a growth factor that may have therapeutic potential in the treatment of ischemic stroke. At this time, however, the postinjury enhancement of neurogenesis appears to offer the best hope for long-lasting functional recovery following brain injury. 相似文献
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