[User benefit of modern hearing aids. A comparative study]. / Gebrauchsnutzen moderner Hörsysteme. Eine vergleichende Studie.

BACKGROUND: In the face of the rapid development of hearing aid system technology it is helpful to regularly study the user benefit of the current generation. TEST PERSONS AND METHODS: To contribute to the question on how the user benefit of current hearing aids compares with the benefit of the previous generation of hearing aids, a multicentre study was carried out in cooperation with 79 hearing aid acoustics companies in Germany. The user benefit of modern hearing aids in everyday life was assessed by asking end users to participate in a survey by completing a questionnaire. The questionnaire consisted of 20 items, 10 of which were taken from validated international inventories (SSQ: Speech, Spatial and Qualities of Hearing scale, IOI-HA: International Outcome Inventory for Hearing Aids) and the other 10 were formulated particularly for this purpose. RESULTS: A total of 664 usable questionnaires were returned whereby 421 responders were first time users and 243 responders were previous hearing aid users. The results of the present study showed that modern hearing aid system technology provides significant extra benefits at the 5 % level relative to the previous generation of hearing aids for all variables tested in this study. CONCLUSIONS: Even though the amount of gain in terms of user benefit may be overestimated due to well-known placebo effects, an obvious net effect was evident. Correlations between the level of hearing aid benefit and possible influencing factors, such as age, gender, subjects own hearing aid, duration of use or hearing loss, could not be identified.

[Effect of frequency compression in hearing aids on speech intelligibility and subjective sound quality]. / Wirkung von Frequenzkompression in Hörgeräten auf das Sprachverstehen und das subjektive Klangempfinden der Nutzer.

BACKGROUND: The acceptance of hearing aids by users with high frequency hearing loss still represents a problem. Processing algorithms that shift high frequency signal components into an audible frequency range are proposed as a solution. We looked into the issue of whether frequency compression becomes more beneficial with increasing high frequency hearing loss or/and for users with cochlear dead regions (DR). SUBJECTS AND METHODS: A total of 20 hearing aid candidates were assessed audiometrically and classified into two test groups in terms of their hearing loss and the presence of DR. The subjects then evaluated four hearing aid settings that differed solely in the degree of frequency compression. Speech recognition threshold measurements and subjective sound quality ratings were carried out for all four settings. RESULTS: Data showed that 15 of the 20 test subjects understood fricatives with a high frequency spectrum component better, since they were able to distinguish between the two logatomes "Afa" and "Asa". No correlation was found between the beneficial effect of frequency compression and the degree of high frequency hearing loss or the presence of DR. Subjective sound quality ratings indicated no clear preference, but excessive frequency compression was generally deemed counterproductive. CONCLUSION: Frequency compression may be appropriate for hearing aid users with high frequency hearing loss and can improve speech recognition. The degree of frequency compression required to achieve maximal benefit varies from case to case and has to be optimized on an individual basis.

Red blood cell-coupled tissue plasminogen activator prevents impairment of cerebral vasodilatory responses through inhibition of c-Jun-N-terminal kinase and potentiation of p38 mitogen-activated protein kinase after cerebral photothrombosis in the newborn pig.

OBJECTIVE: Pediatric ischemic stroke is a poorly understood, yet clinically important, problem. The sole approved treatment for acute stroke is tissue-type plasminogen activator. However, tissue plasminogen activator vasoactivity aggravates hypoxia/ischemia-induced impairment of cerebrovasodilation in response to hypercapnia and hypotension in newborn pigs. Mitogen-activated protein kinase (a family of 3 kinases, extracellular signal-related kinase, p38, and c-Jun-N-terminal kinase) is upregulated after hypoxia/ischemia. Coupling of tissue plasminogen activator to red blood cells prevented hypoxia/ischemia-induced impairment of dilation and suppressed extracellular signal-related kinase mitogen-activated protein kinase activation. This study investigated the differential roles of mitogen-activated protein kinase isoforms in the effects of red blood cells-tissue plasminogen activator on cerebrovasodilation in a translationally relevant injury model, photothrombosis. DESIGN: Prospective, randomized animal study. SETTING: : University laboratory. SUBJECTS: Newborn (1- to 5-day-old) pigs. INTERVENTIONS: Cerebral blood flow and pial artery diameter were determined before and after photothrombotic injury (laser 532 nm and erythrosine B) was produced in piglets equipped with a closed cranial window. Cerebral blood flow extracellular signal-related kinase, p38, and c-Jun-N-terminal kinase mitogen-activated protein kinase were determined by enzyme-linked immunosorbent assay. MEASUREMENTS AND MAIN RESULTS: Tissue plasminogen activator and red blood cells-tissue plasminogen activator alleviated reduction of cerebral blood flow after photothrombotic injury. Cerebrovasodilation was blunted by photothrombotic injury, reversed to vasoconstriction by tissue plasminogen activator, but dilation was maintained by red blood cells-tissue plasminogen activator. Cerebral blood flow c-Jun-N-terminal kinase and p38 mitogen-activated protein kinase but not extracellular signal-related kinase mitogen-activated protein kinase was elevated by photothrombotic injury, an effect potentiated by tissue plasminogen activator. Red blood cells-tissue plasminogen activator blocked c-Jun-N-terminal kinase but potentiated p38 mitogen-activated protein kinase upregulation after photothrombotic injury. A c-Jun-N-terminal kinase mitogen-activated protein kinase antagonist prevented, a p38 mitogen-activated protein kinase antagonist potentiated, whereas an extracellular signal-related kinase mitogen-activated protein kinase antagonist had no effect on dilator impairment after photothrombotic injury. CONCLUSIONS: These data indicate that in addition to restoring perfusion, red blood cells-tissue plasminogen activator prevents impairment of cerebrovasodilation after photothrombotic injury through blockade of c-Jun-N-terminal kinase and potentiation of p38 mitogen-activated protein kinase. These data suggest tissue plasminogen activator coupling to red blood cells offers a novel approach to increase the benefit/risk ratio of thrombolytic therapy to treat central nervous system ischemic disorders.

Use of O-arm With Intraoperative Arteriography for Localization and Stealth Navigation of the Vertebral Arteries During Posterior Cervical Spine Surgery.

BACKGROUND: Vertebral artery injury (VAI) can be a devastating complication during cervical spine surgery. Although considered a rare occurrence overall, incidences of VAI have been reported in the ranges of 0.07% to 8%. Such injuries have the potential for catastrophic consequences, including blood loss, permanent morbid neurologic injury, and even death. The introduction of intraoperative navigation using either preoperative or intraoperative imaging has now been widely adopted in current practice so as to try and minimize adverse outcomes while giving real-time, dynamic information of the operative field. The use of the O-arm Surgical Imaging System during cervical spine surgery allows one to obtain high-resolution, accurate intraoperative imaging, and when used in concert with forms of intraoperative navigation, it can help with instrumentation and safety. However, patients undergoing cervical spine surgery do not routinely undergo preoperative vascular imaging, particularly with regard to anterior cervical or posterior high-cervical surgeries, where the incidence of VAI, in comparison with other cervical surgeries, has been reported to be the highest. METHODS: Here we present the use of intraoperative O-arm-based arteriography for integration with navigation for vertebral artery localization during C1 to C3 posterior instrumentation and fusion of an unstable C2 fracture in a 54-year-old man. RESULTS: The patient did not experience any intraoperative VAI and was subsequently discharged with no focal neurologic deficits. CONCLUSIONS: Detailed in our report is our protocol and procedure for obtaining and using intraoperative angiographic images. CLINICAL RELEVANCE: Case report detailing O arm for intraoperative identification of vertebral arteries during C1-C3 posterior instrumentation and fusion with pre-operative unilateral vertebral artery injury.

Signaling, delivery and age as emerging issues in the benefit/risk ratio outcome of tPA For treatment of CNS ischemic disorders.

Stroke is a leading cause of morbidity and mortality. While tissue-type plasminogen activator (tPA) remains the only FDA-approved treatment for ischemic stroke, clinical use of tPA has been constrained to roughly 3% of eligible patients because of the danger of intracranial hemorrhage and a narrow 3 h time window for safe administration. Basic science studies indicate that tPA enhances excitotoxic neuronal cell death. In this review, the beneficial and deleterious effects of tPA in ischemic brain are discussed along with emphasis on development of new approaches toward treatment of patients with acute ischemic stroke. In particular, roles of tPA-induced signaling and a novel delivery system for tPA administration based on tPA coupling to carrier red blood cells will be considered as therapeutic modalities for increasing tPA benefit/risk ratio. The concept of the neurovascular unit will be discussed in the context of dynamic relationships between tPA-induced changes in cerebral hemodynamics and histopathologic outcome of CNS ischemia. Additionally, the role of age will be considered since thrombolytic therapy is being increasingly used in the pediatric population, but there are few basic science studies of CNS injury in pediatric animals.

PAI-1-derived peptide EEIIMD prevents impairment of cerebrovasodilation by augmenting p38 MAPK upregulation after cerebral hypoxia/ischemia.

Babies are frequently exposed to cerebral hypoxia and ischemia (H/I) during the perinatal period as a result of stroke, problems with delivery, or postdelivery respiratory management. The sole approved treatment for acute stroke is tissue type plasminogen activator. H/I impairs pial artery dilation (PAD) induced by hypercapnia and hypotension, the impairment aggravated by type plasminogen activator and attenuated by the plasminogen activator inhibitor-1-derived peptide EEIIMD. Mitogen-activated protein kinase (MAPK), a family of at least three kinases, ERK, p38, and JNK, is upregulated after H/I and ERK contribute to impaired cerebrovasodilation. This study determined the roles of p38 and JNK MAPK in the impairment of dilation post-H/I in pigs equipped with a closed cranial window and the relationship between alterations in MAPK isoforms and EEIIMD-mediated cerebrovascular protection. Cerebrospinal fluid-phosphorylated (activated) p38 MAPK, but not JNK MAPK, was increased after H/I, an effect potentiated by intravenous EEIIMD administered 1 h postinjury. PAD in response to hypercapnia and hypotension was blunted by H/I, but dilation was maintained by EEIIMD. PAD was further impaired by the p38 antagonist SB-203580 but unchanged by the JNK antagonist SP-600125. Isoproterenol-induced PAD was unchanged by H/I, EEIIMD, SB-203580, and SP-600125. These data indicate that postinjury treatment with EEIIMD attenuated impaired cerebrovasodilation post-H/I by upregulating p38 but not JNK. These data suggest that plasminogen activator inhibitor-1-based peptides and other approaches to upregulate p38 may offer a novel approach to increase the benefit-to-risk ratio of thrombolytic therapy for diverse central nervous system disorders associated with H/I.

Impaired cerebral blood flow autoregulation during posttraumatic arterial hypotension after fluid percussion brain injury is prevented by phenylephrine in female but exacerbated in male piglets by extracellular signal-related kinase mitogen-activated protein kinase upregulation.

OBJECTIVE: Traumatic brain injury contributes to morbidity and mortality in children and boys are disproportionately represented. Hypotension is common and worsens outcome after traumatic brain injury. Extracellular signal-related kinase mitogen-activated protein kinase is upregulated and reduces cerebral blood flow after fluid percussion brain injury in piglets. We hypothesized that increased cerebral perfusion pressure through phenylephrine sex dependently reduces impairment of cerebral autoregulation during hypotension after fluid percussion brain injury through modulation of extracellular signal-related kinase mitogen-activated protein kinase. DESIGN: Prospective, randomized animal study. SETTING: University laboratory. SUBJECTS: Newborn (1- to 5-day-old) pigs. INTERVENTIONS: Cerebral blood flow, pial artery diameter, intracranial pressure, and autoregulatory index were determined before and after fluid percussion brain injury in untreated, preinjury, and postinjury phenylephrine (1 microg/kg/min intravenously) treated male and female pigs during normotension and hemorrhagic hypotension. Cerebrospinal fluid extracellular signal-related kinase mitogen-activated protein kinase was determined by enzyme-linked immunosorbent assay. MEASUREMENTS AND MAIN RESULTS: Reductions in pial artery diameter, cerebral blood flow, cerebral perfusion pressure, and elevated intracranial pressure after fluid percussion brain injury were greater in males, which were blunted by phenylephrine pre- or postfluid percussion brain injury. During hypotension and fluid percussion brain injury, pial artery dilation was impaired more in males. Phenylephrine decreased impairment of hypotensive pial artery dilation after fluid percussion brain injury in females, but paradoxically caused vasoconstriction after fluid percussion brain injury in males. Papaverine-induced pial artery vasodilation was unchanged by fluid percussion brain injury and phenylephrine. Cerebral blood flow, cerebral perfusion pressure, and autoregulatory index decreased markedly during hypotension and fluid percussion brain injury in males but less in females. Phenylephrine prevented reductions in cerebral blood flow, cerebral perfusion pressure, and autoregulatory index during hypotension in females but increased reductions in males. Cerebrospinal fluid extracellular signal-related kinase mitogen-activated protein kinase was increased more in males than females after fluid percussion brain injury. Phenylephrine blunted extracellular signal-related kinase mitogen-activated protein kinase upregulation in females but increased extracellular signal-related kinase mitogen-activated protein kinase upregulation in males after fluid percussion brain injury. CONCLUSIONS: These data indicate that elevation of cerebral perfusion pressure with phenylephrine sex dependently prevents impairment of cerebral autoregulation during hypotension after fluid percussion brain injury through modulation of extracellular signal-related kinase mitogen-activated protein kinase. These data suggest the potential role for sex-dependent mechanisms in cerebral autoregulation after pediatric traumatic brain injury.

Novel plasminogen activator inhibitor-1-derived peptide protects against impairment of cerebrovasodilation after photothrombosis through inhibition of JNK MAPK.

The sole FDA-approved treatment for acute stroke is recombinant tissue-type plasminogen activator (rtPA). However, rtPA aggravates the impairment of cerebrovasodilation induced by global hypoxia/ischemia; this impairment is attenuated by the preinjury treatment with the plasminogen activator inhibitor derivative EEIIMD. MAPK (a family of kinases, p38, and JNK) is upregulated after cerebral ischemia. In this study, we determined whether the novel plasminogen activator inhibitor-derived peptide, Ac-RMAPEEIIMDRPFLYVVR-amide, (PAI-1-DP) given 30 min before or 2 h after, focal central nervous system injury induced by photothrombosis would preserve responses to cerebrovasodilators and the role of p38 and JNK MAPK in such effects. Cerebrospinal fluid JNK and p38 levels were elevated by photothrombotic injury, an effect potentiated by rtPA. Cerebrovasodilation was blunted by photothrombosis and reversed to vasoconstriction by rtPA but restored to dilation by PAI-1-DP pre- and posttreatment. PAI-1-DP blocked JNK, but preserved p38 MAPK upregulation after photothrombosis. The JNK MAPK antagonist SP600125 prevented, and the p38 antagonist SB203580 potentiated, impaired cerebrovasodilation after photothrombosis. These data indicate that rtPA impairs cerebrovasodilation after injury by activating JNK, while p38 MAPK is protective, and that the novel peptide PAI-1-DP protects by inhibiting activation of JNK by rtPA. JNK MAPK inhibitors, including PAI-1-DP, may offer a novel approach to increase the benefit-to-risk ratio of thrombolytic therapy and enable its use in central nervous system ischemic disorders.

Cascaded optical parametric oscillations generating tunable terahertz waves in periodically poled lithium niobate crystals.

We present a continuous-wave (cw) singly-resonant optical parametric oscillator (SROPO) based on MgO-doped periodically poled lithium niobate (PPLN) delivering single-frequency idler output from 2.33 to 5.32 microm. In this system, we observe additional spectral components that have been attributed to stimulated Raman lines in other studies. However, we are able to assign them unambiguously to cascaded optical parametric processes. The tunable forward and backward idler waves generated by these additional phase-matched oscillations have frequencies that are tunable around 3.5 and 1.5 THz, respectively.

Visualization of a cytoskeleton-like FtsZ network in chloroplasts.

It has been a long-standing dogma in life sciences that only eukaryotic organisms possess a cytoskeleton. Recently, this belief was questioned by the finding that the bacterial cell division protein FtsZ resembles tubulin in sequence and structure and, thus, may be the progenitor of this major eukaryotic cytoskeletal element. Here, we report two nuclear-encoded plant ftsZ genes which are highly conserved in coding sequence and intron structure. Both their encoded proteins are imported into plastids and there, like in bacteria, they act on the division process in a dose-dependent manner. Whereas in bacteria FtsZ only transiently polymerizes to a ring-like structure, in chloroplasts we identified persistent, highly organized filamentous scaffolds that are most likely involved in the maintenance of plastid integrity and in plastid division. As these networks resemble the eukaryotic cytoskeleton in form and function, we suggest the term "plastoskeleton" for this newly described subcellular structure.

Hybridly-pumped continuous-wave optical parametric oscillator.

We present the first to our knowledge continuous-wave singly-resonant optical parametric oscillator (SROPO) generating tunable signal and idler waves with less than 100 mW single-frequency pump power. This low threshold is achieved by an additional intracavity gain medium that is pumped incoherently. The idler power with respect to the single-frequency pump power shows a bistable behavior which depends strongly on the pumping of the additional amplifier. Furthermore, we demonstrate that such a setup allows a SROPO to be completely diode pumped.

Traumatic Frontal Epidural Hematoma Caused by Multiple Arterial Injuries in the Anterior Fossa.

BACKGROUND: This case report illustrates the need to evaluate the possibility of multiple arterial sources when presented with a frontal epidural hematoma associated with facial trauma. CASE DESCRIPTION: The patient presented after being struck in the face by a baseball. Computed tomography of the brain revealed a large frontal epidural hematoma. Intraoperatively, bleeding from a frontal branch of the middle meningeal artery was encountered and cauterized, and the hematoma was removed. Routine follow-up imaging performed the next day showed a residual frontal hematoma; however, the epidural hematoma was in a more medial location than the initial hematoma. The patient was taken back to the operating room; after frontal lobe retraction and extensive exploration, a different source of bleeding from posterior ethmoidal artery feeders was encountered. After the second operation, the patient's hematoma did not recur, and he was discharged home with no neurologic deficits 3 days later. CONCLUSIONS: We report a case of an epidural hematoma caused by 2 distinct arterial feeders. We discuss radiologic review and operative management of anterior fossa epidural hematomas and stress the importance of considering arterial bleeding from sources other than the middle meningeal artery in anterior fossa epidural hematomas. We discuss the utility of preoperative angiography for these patients and reinforce the need for acute postoperative imaging to ensure successful operative and patient outcomes.

Rickettsia spp. in Ixodes ricinus ticks in Bavaria, Germany.

This study aims to provide information on the occurrence of spotted fever rickettsiae in Ixodes ricinus ticks in southern Germany. A total of 2,141 I. ricinus ticks was collected in Bavaria. Pools of 5-10 ticks were studied by a PCR targeting the rickettsial citrate synthase gene gltA. The average prevalence rate was 12% (257 of 2,141). Sequencing data exclusively identified Rickettsia helvetica DNA. Results and other data demonstrate the possible role of R. helvetica in I. ricinus as a source of human infections in southern Germany.

Angioscopy in endovascular surgery: recent technical advances to enhance intervention selection and failure analysis.

Recent technical and procedural modifications have greatly enhanced the usefulness of angioscopy during angioplasty. A pulsed irrigation system, proximal and distal blood flow control by pressure, and attention to sheath/vessel diameter ratio were incorporated into a study in which angioscopy was used for pretreatment assessment in 23 patients with symptomatic peripheral vascular disease presenting for initial (8 patients) evaluation or repeat treatment (15 patients) following a previous vascular procedure. Twenty-five lesions were examined with a 2.3 mm flexible angioscope equipped with an irrigating lumen; there were no complications attributable to angioscopy. The angioscope was useful in the characterization of lesions for selection of the recanalization technique. Lesions more amenable to initial atherectomy were visualized in 12 patients; 7 occlusions were successfully treated with laser/balloon angioplasty, with angioscopy assisting in probe and/or wire passage in 4 cases. Three late reocclusions were identified angioscopically as due solely to thrombosis, indicating the need for thrombolytic therapy. Angioscopy also identified 4 cases of incomplete recanalization despite a satisfactory arteriographic image. Angioscopy was also used to evaluate stenotic lesions unaccompanied by thrombus formation in patients previously treated with laser-assisted angioplasty. Histologic evaluation of the biopsied plaques identified intimal hyperplasia as the etiology, matching identically similar specimens harvested from a lesion treated with balloon dilation only.

Intraoperative coronary excimer laser angioplasty: preliminary clinical experience.

Diffuse coronary artery atherosclerosis is generally recognized as a deterrent to successful revascularization if it cannot be adequately treated. Mechanical endarterectomy can be useful, but it is not the optimal solution owing to the associated higher incidences of perioperative infarction and mortality. The use of laser energy as an endarterectomy tool appears promising. To investigate the application of excimer laser radiation to intraoperative coronary artery endarterectomy, 15 stenotic lesions in 13 patients were treated with excimer irradiation during coronary artery bypass grafting. Eleven (73%) of the lesions were enlarged by the excimer probe (6 of the successes were in calcified lesions). The 4 arteries not enlarged by the excimer laser all demonstrated calcified lesions. There were 3 perforations and 2 dissections, all but 1 in heavily calcified arteries. The results of this phase 1 safety and efficacy study indicate that excimer irradiation can recanalize most arteries, including total and subtotal occlusions and some calcified lesions. Further evaluation with better delivery systems is needed to determine whether the perforation rate can be reduced.

[The usefulness of today's hearing aids--possibilities and limitations]. / Was Hörgeräte heute leisten--Möglichkeiten und Grenzen.

Some ten to twelve million people in Germany are estimated to need hearing aids. Many of the hard of hearing suffer from inner ear deafness with hair cell dysfunction, and not only hear sounds at too low a level of intensity, but also distorted and unintelligible. Modern special digital hearing aids are able, by appropriate amplification of certain frequencies or frequency bands or, e.g. through the use of directional microphones, to improve discrimination of speech from surrounding noise. In patients with mild hearing losses in particular, the use of bilateral hearing aids is recommended to improve speech recognition. Attention is drawn to the importance of individual counselling and the testing of the hearing aids by the patient.

Glucagon protects against impaired NMDA-mediated cerebrovasodilation and cerebral autoregulation during hypotension after brain injury by activating cAMP protein kinase A and inhibiting upregulation of tPA.

Outcome of traumatic brain injury (TBI) is impaired by hyperglycemia, hypotension, and glutamate, and improved by insulin. Insulin reduces glutamate concentration, making it uncertain whether its beneficial effect accrues from euglycemia. Glucagon decreases CNS glutamate, lessens neuronal cell injury, and improves neurological scores in mice after TBI. In vitro, glucagon limits NMDA-mediated excitotoxicity by increasing cAMP and protein kinase A (PKA). NMDA receptor activation couples cerebral blood flow (CBF) to metabolism. Dilation induced by NMDA is impaired after fluid percussion brain injury (FPI) due to upregulation of endogenous tPA, which further disturbs cerebral autoregulation during hypotension after fluid percussion injury (FPI). We hypothesized that glucagon prevents impaired NMDA receptor-mediated dilation after FPI by upregulating cAMP, which decreases release of tPA. NMDA-induced pial artery dilation (PAD) was reversed to vasoconstriction after FPI. Glucagon 30 min before or 30 min after FPI blocked NMDA-mediated vasoconstriction and restored the response to vasodilation. PAD during hypotension was blunted after FPI, but protected by glucagon. Glucagon prevented FPI-induced reductions in CSF cAMP, yielding a net increase in cAMP, and blocked FPI-induced elevation of CSF tPA. Co-administration of the PKA antagonist Rp 8Br cAMPs prevented glucagon-mediated preservation of NMDA-mediated dilation after FPI. The pKA agonist Sp 8Br cAMPs prevented impairment of NMDA-induced dilation. These data indicate that glucagon protects against impaired cerebrovasodilation by upregulating cAMP, which decreases release of tPA, suggesting that it may provide neuroprotection when given after TBI, or prior to certain neurosurgical or cardiac interventions in which the incidence of perioperative ischemia is high.

Phenylephrine infusion prevents impairment of ATP- and calcium-sensitive potassium channel-mediated cerebrovasodilation after brain injury in female, but aggravates impairment in male, piglets through modulation of ERK MAPK upregulation.

Traumatic brain injury (TBI) contributes to morbidity in children and boys, and hypotension worsens outcome. Extracellular signal-related kinase (ERK) mitogen-activated protein kinase (MAPK) is upregulated more in males and reduces cerebral blood flow (CBF) after fluid percussion injury (FPI). Increased cerebral perfusion pressure (CPP) via phenylephrine (Phe) sex-dependently improves impairment of the cerebral autoregulation seen after FPI through modulation of ERK MAPK upregulation, which is aggravated in males, but is blocked in females. Activation of ATP- and calcium-sensitive (Katp and Kca) channels produces cerebrovasodilation and contributes to autoregulation, both of which are impaired after FPI. Using piglets equipped with a closed cranial window, we hypothesized that potassium channel functional impairment after FPI is prevented by Phe in a sex-dependent manner through modulation of ERK MAPK upregulation. The Katp and Kca agonists cromakalim and NS 1619 produced vasodilation that was impaired after FPI more in males than in females. Phe prevented reductions in cerebrovasodilation after cromakalim and NS 1619 in females, but reduced dilation after these potassium channel agonists were given to males after FPI. Co-administration of U 0126, an ERK antagonist, and Phe fully restored dilation to cromakalim, calcitonin gene-related peptide (CGRP), and NS 1619, in males after FPI. These data indicate that Phe sex-dependently prevents impairment of Katp and Kca channel-mediated cerebrovasodilation after FPI in females, but aggravates impairment in males, through modulation of ERK MAPK upregulation. Since autoregulation of CBF is dependent on intact functioning of potassium channels, these data suggest a role for sex-dependent mechanisms in the treatment of cerebral autoregulation impairment after pediatric TBI.